FAQ

FAQ: Common Questions and Common Failure Modes

Prefer verifiable progress to flashy conclusions

Mind Uploading Research Project

Public Page Updated: 2026-04-04 Human-first

How to use this page

Read this first to avoid getting lost

This page is a Q&A for the questions many readers hit first when reading Mind-Upload. It stays short as an entry point, but every strong claim is tied back to a page with evidence.

  • It quickly clears up first-order questions such as what this site is for and what EEG or brain-to-text work can and cannot support.
  • At the front door, invasive language BCIs are now split into same-session communication throughput, cross-subject transfer / initialization, fixed-decoder durability slices, and adaptive rescue routes instead of one `speech BCI success` label.
  • At the FAQ front door, EEG foundation-model evidence is now split into representation learning / efficiency, recording-frame compatibility, label-limited adaptation rescue, and benchmark governance / postmortem rather than one `general decoder progress` ladder.
  • At the FAQ front door, `harmonized EEG` is no longer one checkbox: common-channel intersection, interpolation to a target montage, and REST-based transformation preserve different measurement objects and ceilings.
  • It now front-loads eleven technical guardrails: connectome-complete is not state-complete, human proxy-rich evidence is not automatically near-direct whole-brain state readout, same-brain functional connectomics / digital-twin language is not automatically a solved local twin because sequential bridge, label source, current synaptic-state ceiling, presynaptic release-machinery ceiling, and dynamical identifiability remain separate conditions, same-subject / same-brain wording does not by itself make a sequential workflow one state sample because carried object / witness, tolerance rule, and rescue route remain separate conditions, a high score is not automatically a target-specific neural readout, a foundation-model or leaderboard result is not automatically a general neural decoder because benchmark object, coordinate route / reference family, adaptation regime or label budget, and benchmark governance remain separate conditions, EEG / MEG connectivity labels are not automatically leak-proof communication maps or causal circuits, BOLD / fNIRS differences need vascular-state / CVR audit, DCM / effective-connectivity labels do not by themselves identify true causal wiring because observed-subsystem closure, node-definition policy, latent-confound audit, and sampling / transformation sensitivity remain separate conditions, thermodynamic / irreversibility labels do not by themselves measure physical dissipation or WBE-ready cost, and low latency does not by itself solve the body / environment boundary.
  • Human proxy bundles are now read on three axes first: proxy class, operational maturity, and calibrator role, and even after that they still need a three-gate composition check for robustness, effective-window / regime compatibility, and increment plus disagreement handling.
  • Sleep replay evidence is not one class either: phase-locked auditory stimulation, endogenous scalp decoding, intracranial closed-loop synchrony, spindle-locked ripple evidence, sleep-integrity or disturbance effects, NREM physiology gating, and item-selective / difficulty-selective or age-dependent TMR effects are not one mechanistic rung.
  • Post-transcriptional RNA evidence is not one class at the FAQ front door either: splice-isoform control, m6A-dependent translation, m6A-dependent degradation, RNA editing, and atlas ceilings are not one inferential object.
  • A chemical connectome plus nominal inhibitory edges still does not fix gap-junction coupling, endogenous field effects, extracellular-space geometry / diffusion barriers / osmotic regime, or local inhibitory driving force.
  • It also keeps one extra asymmetry visible: the strongest maintenance-state causal papers and the best current human-observability papers are often different ladders.
  • It now makes one asymmetry concrete at the front door: rodent astrocyte / lymphatic causality, human SMBT-1 MAO-B target-validation / AD-context / brain-quantification / whole-body-biodistribution routes, human SL25.1188 MAO-B disease / severity routes, human I2BS PET, human TSPO disease-context / pathology-validated PET, human CSF1R first-in-human route-setting PET, human COX-2 celecoxib-blockade / test-retest-bounded enzyme PET, choroid-plexus perfusion, blood-to-CSF transport, choroid-plexus water cycling, apparent BCSFB exchange, macroscopic CSF oscillation, parenchyma-CSF water exchange, respiration-conditioned net flow, exercise-conditioned contrast influx / meningeal-lymphatic flow, intrathecal tracer / CSF-to-blood clearance, CSF mobility, and model-based biomarker efflux are kept on separate rows rather than one progress bar.
  • It also keeps measurement-side vascular-state / CVR audit separate from maintenance-side neurovascular-unit / BBB / pericyte state, and keeps BBB water-exchange, tracer-specific BBB transport, and blood-CSF barrier / choroid-plexus perfusion / transport / water-cycling / apparent-exchange routes distinct from both BBB causality and clearance routes.
  • If a connectome claim is diffusion-MRI-derived, acquisition scheme, endpoint assignment, graph construction, and uncertainty route all change what the object means; this FAQ now stops that overread at the front door.
  • It avoids dramatic overstatement and states what remains unresolved at the same time.
  • It is structured so readers can tell when the FAQ is enough and when they should move on to the full page.
Best for
Readers who want to sort out questions and misconceptions first, and readers who want a quick overview through short Q&A
Reading time
8-15 minutes
Accuracy note
This page gives short answers. Please do not quote the conclusion alone; return to the linked pages and references when you need the full basis.

Relatively clear at this stage

What we know now

  • Even short Q&A becomes much safer when strong claims are decomposed into weaker, more testable claims.
  • The impressive appearance of EEG or LLM outputs must be separated from strong WBE claims, and the contributions of language priors, nuisance routes, and brain-derived information must also be separated.
  • For foundation / self-supervised EEG models, benchmark object, pretraining-corpus identity, coordinate route / reference family, adaptation regime or label budget, and benchmark governance can all change what a score means, so a leaderboard result is not automatically a general neural decoder.
  • Recent EEG foundation-model benchmarks still show regime-dependent trade-offs: narrow-source checkpoints can win linear probes while more diverse pretraining can win after fine-tuning, so model rank is not one monotonic capability scale.
  • For invasive language BCIs, same-session throughput, transfer-assisted initialization, fixed-decoder durability, and adaptive rescue are different operational claims.
  • Same-brain functional connectomics and stimulus-conditioned digital-twin models are not one solved local-twin class; bridge class, label-transfer route, synaptic-state ceiling, presynaptic release-machinery ceiling, and dynamical degeneracy remain separate questions.
  • For same-subject / same-brain bridges, landmarks, latent manifolds, representational geometry, and fingerprint features are different carried objects, and stable scores can still depend on alignment, recalibration, or a short fixed-decoder horizon.
  • Because wiring diagrams and cell types still leave excitability, timing-state, thermal-state, transcription/chromatin, post-transcriptional RNA-state, phospho-signaling / second-messenger state, proteostasis, cargo-transport / cytoskeletal trafficking state, ECM / PNN, ionic-homeostasis, bioenergetic / mitochondrial state, glial substrate-routing, astrocyte-state, clearance / immune support, and other maintenance-support variables unresolved, long-term dynamical claims require separate auditing.
  • Sleep history and sleep architecture / replay-coupling are different variables, and even within sleep replay, phase-locked stimulation, endogenous scalp decoding, intracranial synchrony interventions, spindle-locked ripple evidence, sleep-integrity burden, NREM physiology gating, and item-selective or age-dependent TMR do not support the same claim.
  • A chemical connectome plus nominal inhibitory edges still does not make fast synchrony, oscillatory coordination, local extracellular dilution regime, or local electrotonic regime solved.
  • For several maintenance-state families, local causal evidence and living-human observability remain misaligned, so a human proxy does not by itself mean the causal controller was measured.
  • The same mismatch now applies to neurovascular support: pericyte / BBB causality, human BBB water-exchange MRI, tracer-specific BBB transport PET, and blood-CSF barrier / choroid-plexus perfusion / transport / water-cycling / apparent-exchange routes are different evidential rows, so vascular audit does not by itself identify the responsible neurovascular or choroid-plexus controller.
  • Rodent astrocyte causality plus human astrocyte / neuroimmune / clearance proxies still do not identify the responsible human controller because target class, evidence role, direct observable, spatial unit, and model burden still differ.
  • Adolescent, healthy-younger, healthy-older, and AD-continuum proxy routes do not define one shared human baseline unless transfer conditions are stated explicitly.
  • Proxy class, operational maturity, and calibrator role are different questions; a real human route may still calibrate only one bounded hidden-state family.
  • Even after proxy class, maturity, and calibrator role are logged, a human proxy bundle still needs a robustness gate, an effective-window / regime-compatibility gate, and an increment-plus-disagreement gate before same-subject state-identification language is allowed.
  • Destructive local ultrastructure and living-human in vivo proxy routes raise different measurement classes and different route burdens, so local ultrastructure, SV2A PET, five-metabolite 1H-MRSI similarity, high-resolution 1H-MRSI metabolite-distribution mapping, 31P metabolite / pH balance, 31P MT exchange-flux, 31P NAD-content mapping, localized functional 31P NAD-dynamics, deuterium absolute metabolite mapping / quantification, deuterium kinetic-rate imaging, tract-scale transmission-speed estimation, myelin-bilayer mapping, BBB water-exchange, tracer-specific BBB transport, blood-CSF barrier / choroid-plexus perfusion / transport / water-cycling / apparent-exchange, astrocyte target / route-role PET, neuroimmune target families, and clearance-transport route families should not be compressed into one progress bar.
  • A human tractography connectome is not one stable graph by default; hubness, laterality, and bundle recovery can move with endpoint policy, filtering, voxel size, q-space sampling, and uncertainty handling.
  • Same-subject or same-brain wording does not by itself make a live-to-fix, cross-regime, or cross-day workflow one state sample; bridge delay, regime continuity, coordinate transfer, and bridge validation still matter.
  • An EEG / MEG connectivity label does not by itself show leak-free inter-areal communication or causality; volume conduction, source leakage, ghost interactions, and pipeline dependence still matter.
  • A BOLD or fNIRS amplitude difference without vascular-state / CVR or short-separation auditing is still not a clean neural difference.
  • A DCM or effective-connectivity label does not by itself discover the one true causal circuit; candidate model space, observed-subsystem closure / latent-confound audit, node-definition policy, sampling / transformation sensitivity, validation, and reliability remain separate requirements.
  • An irreversibility / entropy-production label does not by itself tell you the coarse-graining, hidden-degree risk, timescale, estimator family, or dynamical assumptions behind the number, and it is not automatically a metabolic-cost readout.
  • A closed-loop demo without a disclosed body / environment boundary, including slow internal-milieu disclosure, remains a local controller or subsystem-loop result rather than evidence that embodiment is solved.
  • FAQ works well as an entry point for avoiding the wrong direction.

Still unresolved beyond this point

What we still do not know

  • Short answers alone cannot settle theory choice or identity questions.
  • How far any individual research result generalizes depends on the original paper and its verification conditions.

Learn the basics

Check the basics in the wiki

How To Read

This page is designed to block common misunderstandings early. The stronger the claim, the more carefully you should check, in order, (1) the definition of terms, (2) the measurement scale, (3) the condition that would count as failure, and (4) the reproduction procedure.

Limits of the FAQ

The FAQ gives short answers so you do not head in the wrong direction first. It is meant to establish orientation; once you need evidence or detail, move on to the linked pages.

When you are not sure where to return after a short answer

The FAQ is only an entry point, so after reading it you still need to decide whether to go next to Verification, WBE 101, Datasets, or the Glossary. If you want the role differences among the public pages first, see Wiki: Guide to the public pages.

When you are unsure how to use the site as a whole

If you want to use the FAQ as the front door and then decide whether to get the overview, study in the wiki, or turn a question into an Issue, see Wiki: The three ways to use this site.

When you are unsure how to read the header guidance and the known/unknown blocks

The blocks at the top of this page, such as how to read the page, the accuracy note, what is known now, and the wiki routes, are there to prevent short Q&A answers from being misread. If you want the shared rules in one place, see Wiki: How to read the public-page header blocks.

When your question is stuck somewhere between L0 and L5

The questions in this FAQ span everything from L0 practical work to L5 social deployment. If you want the next pages organized by claim level, see Wiki: Reading routes for L0-L5.

When you are unsure whether to follow theory pages or practical pages next

If you want to continue only into theory pages after the FAQ, see Wiki: Guide to the theory pages. If you want to continue into practical pages such as Verification or Datasets, see Wiki: Guide to the practical pages.

When you are unsure which page to open after Verification

If you move from the FAQ into Verification and then are unsure whether to return to L0 implementation or jump first to L2, L3, or L4, see Wiki: Four paths after Verification.

When you want to turn the question itself into an Issue

If reading the FAQ makes you think “this is unclear” or “this condition is missing,” and you want to turn that directly into a useful Issue, see Wiki: Writing your first Issue.

When you understand the meaning but not the next action

If the FAQ helped you understand the topic but you still do not know what to verify next before making a correction or judgment, see Wiki: The difference between understanding and being ready to act.

Eleven technical guards now fixed at the front door

This FAQ now blocks eleven fast overreads before they spread through the site: connectome-complete is not state-complete, human proxy-rich evidence is not automatically near-direct whole-brain state readout, same-brain functional connectomics / digital-twin language is not automatically a solved local twin, same-subject / same-brain is not automatically same-state in a sequential bridge, high score is not automatically target-specific neural evidence, a foundation-model or leaderboard result is not automatically a general neural decoder, sensor- or source-space connectivity is not automatically a leak-proof communication map or causal circuit, BOLD / fNIRS amplitude difference is not automatically a neural difference without vascular-state / CVR audit, DCM / effective-connectivity output is not automatically the brain's true causal wiring, thermodynamic / irreversibility labels are not automatically direct physical-dissipation measurements or WBE gates, and low latency is not automatically a solved body / environment boundary. The human-proxy stop rule is now narrower as well: even after proxy class, operational maturity, and calibrator role are named, the bundle still has to pass a robustness gate, an effective-window / physiological-regime compatibility gate, and an increment-over-the-strongest-single-row gate with disagreement handling. The bridge-specific stop rule is now narrower as well: same-subject solves specimen identity only, whereas carried object / witness, tolerance / failure rule, and rescue route still have to be named before same-state language is allowed. For same-brain functional connectomics, the extra stop rule is that bridge class, label source, current synaptic-state ceiling, presynaptic release-machinery ceiling, and dynamical identifiability still have to be named before local-twin language is allowed. If you need the full rule set behind them, go next to EEG 101, Verification: Pretraining Card, Verification: Specificity & Shortcut Card, Verification: Observability Budget, Verification: State-Continuity Bridge Card, Verification: Body / Environment Boundary Card, Wiki: Why a Connectome Is Not Enough, Wiki: Observability and Claim Ceiling by Measurement Stack, Wiki: State-Continuity Bridge, Wiki: effective-connectivity route card, and Wiki: irreversibility route card.

If you want to... Read this question first
Know only what this site is for Start with Q0, “What does Mind-Upload actually do?” for the fastest overview.
Avoid misreading flashy claims in news coverage Read the Q1 series first to separate task-limited decode, shortcut routes, foundation-model / benchmark-governance overreads, connectivity-ceiling issues, hemodynamic proxy limits, model-conditioned causal claims, and thermodynamic overreads before moving on to Q2.
Know only what counts as progress Q3, “Then what should we build to count as progress?” shows the minimum deliverables for L0-L2.
Know whether the connectome alone is enough Q2c, “If we know the connectome and cell type, is the rest mostly filled in?” clarifies which hidden-state families remain outside connectome plus cell type.
Know whether same-brain connectomics solved a local twin Q2c1, “If same-brain functional connectomics or a digital twin works, did we solve a local twin?” separates scaffold progress from transcriptomic truth, current synaptic-state readout, presynaptic release-machinery readout, and unique dynamics.
Know what humans can actually observe today Q2d, “If human measurement keeps improving, are we close to state-complete readout?” separates proxy class from route maturity before you overread human evidence.
Know whether same-subject or same-brain really means one state sample Q2e, “If a paper says same-subject or same-brain, does that mean one state was captured?” separates specimen identity from bridge validity.
Know whether a foundation-model or leaderboard result means a general decoder Q1c2, “If a foundation-model or leaderboard result is strong, did we solve general EEG decoding?” separates benchmark object, recording-frame assumptions, adaptation regime, and benchmark governance from the headline score.
Know the conditions for real-time or closed-loop work Start with Q5b, “If offline accuracy is high, is that enough for closed loop?” to see what L3 adds.
Know the philosophical or ethical positions involved Read Q6 on the hard problem and Q9 on ethics to see what the site does and does not claim there.
Four checks for strong claims
  1. What was actually achieved? Check which level from L0 to L5 the claim belongs to.
  2. What was actually measured? Separate output matching from intervention or counterfactual testing.
  3. What would count as being wrong? Look for an explicit falsification condition.
  4. Can other people follow it? Check whether the data, code, logs, and procedure are public.

Q. What does Mind-Upload actually do?

A. It is a site for building a Verification Commons that turns mind uploading and WBE into a verifiable research program. It fixes the data inputs, evaluation outputs, rules for success and failure, and operational procedures first.

Start

The overall picture starts here.

Open Verification →

Q. Can EEG read “thoughts”?

A. It is fair to say that some aspects can be read under constrained conditions, but it is not yet fair to say that free thought can be read as such. The reason is that the strongest non-invasive papers do not all solve the same problem. Tang et al. (2023) demonstrated subject-cooperative semantic reconstruction from within-subject fMRI. Défossez et al. (2023) showed 3 s speech-segment identification from non-invasive M/EEG with predictions dominated by lexical and contextual representations. d'Ascoli et al. (2025) showed known-word-onset decoding across 723 people and roughly five million words, but performance still depended strongly on task structure, with MEG and reading outperforming EEG and listening. Ye et al. (2025) then showed prompt-conditioned fMRI-to-LLM generation that beat a permuted-brain control, but still depended heavily on prompt and LLM scaffold.

Another correction is needed at the task-design layer itself. Rybár et al. (2024) showed that EEG semantic-category decoding can reach mean accuracies up to 71.3% during cue presentation while failing to decode the same categories during the later, cue-separated mental-task period. So a paper that mixes cue-period data with internally generated processing can overstate the communication ceiling before any decoder architecture is discussed. Horikawa (2025) then added a different non-invasive route again: whole-brain fMRI was linearly decoded into semantic features and iteratively optimized into captions of viewed or recalled videos. That is a viewed/recalled content captioning route, not the same object as continuous language reconstruction, known-onset word decoding, or free-running language production.

It is also not the case that scalp signals uniquely determine the internal state. In Unnwongse et al. (2023), which used intracranial stimulation for direct validation, the mean ESI localization error ranged from 10.3 to 26.0 mm depending on source depth and skull conductivity. In Hao et al. (2025), using simultaneous HD-EEG and SEEG, ictal ESI outperformed interictal ESI, but the figures were still 14.07 ± 4.62 mm versus 17.38 ± 4.16 mm, and accuracy depended strongly on source depth and spike power.

There is also an earlier limit than the inverse solver: not every neural pattern creates a usable scalp field. Ahlfors et al. (2010) showed that sensitivity already changes with source orientation, Ahlfors et al. (2010) showed that extended sources can cancel at the surface, Goldenholz et al. (2009) showed that anatomy and source extent can shift SNR by around 10 dB in mesial temporal examples, and Piastra et al. (2021) showed that omitting CSF overestimates EEG sensitivity. So a prettier map or more channels do not by themselves create observability that field formation never provided.

On this site, we therefore do not treat “externally validated ESI” as one checkbox. Intracranial-stimulation ground truth, simultaneous HD-EEG/SEEG, and postsurgical outcome answer different error questions, so the benchmark class has to be named before the claim ceiling is raised. The shortest route is EEG 101: what must now be stated rigorously about ESI and Datasets: the source-imaging validation ladder.

Another weak reading is to publish only the cleanest inverse map and silently ignore how much the answer moves across reasonable pipelines. Mahjoory et al. (2017) showed that inverse-method and software-package choice can materially change source localization and even more strongly change downstream connectivity estimates. Mikulan et al. (2020) then showed on a ground-truth intracranial-stimulation benchmark that many tested parameter combinations miss the session-wise optimum by a wide margin. So at Mind-Upload, one pretty ESI map without cross-solver / cross-parameter spread or an uncertainty display is still read as method-sensitive evidence, not as a stable source fact.

The Mind-Upload position is not to deny ambitious readout work. It is to separate the claim first into task-dependent decoding and internal-state identification, then make explicit the language prior, calibration, abstention conditions, and whether direct validation exists. If you skip those distinctions, you end up misreading “a string was produced” as if it were WBE-relevant state reconstruction.

Do not collapse Q1 into one sentence

A string came out, it came out from brain-derived information alone, the score followed the target variable rather than shortcut routes, and the internal state was identified are different claims. When reading brain-to-text work, separate (1) the measurement method, (2) the task constraints, (3) the language prior, (4) the presence or absence of direct validation, (5) shortcut and nuisance-route auditing, and (6) calibration and abstention conditions.

Q. What is the minimum you should check in a brain-to-text demo?

A. At minimum, check the following eleven things.

  • Measurement method: scalp EEG, MEG, fMRI, ECoG, or intracortical array. Representative high-performance speech neuroprostheses are invasive.
  • Task: heard words, read words, speech articulation, recall, or free conversation. A constrained perceptual task is not the same as free thought.
  • Cue regime: whether the paper decodes cue presentation, externally supported perception, or a cue-separated self-generated mental period. Cue-period performance is not the same thing as self-generated semantic BCI performance.
  • Timing and segmentation: known word onset, fixed multi-second segment, fMRI TR window, prompted continuation, or free-running onset detection. Known onset is not the same thing as unconstrained decoding.
  • Output family: fixed-bank segment retrieval, known-onset word decoding, prompt-conditioned generation, viewed/recalled content captioning, or streaming attempted-speech synthesis. These outputs do not share one uncertainty object.
  • Priors and baselines: fixed vocabulary, beam search, external corpora, LLMs, prompt length, and how far LM-only, no-brain, permuted-brain, no-text-prompt, or shuffle baselines were used. Fluency does not automatically reflect brain signal alone.
  • Validation: held-out conditions, counterfactual tests, adversarial controls, and whether failure cases are shown. Evaluation that stays too close to the training setup is not strong evidence.
  • Subject route: within-subject, cross-subject, adapted-to-subject, or zero-shot to unseen people, together with any cooperation requirement or countermeasure test.
  • Operational route: same-session throughput / expressivity, transfer-assisted initialization, fixed-decoder durability, and adaptive rescue answer different questions. Do not collapse them into one `speech BCI` score.
  • Confidence handling: whether confidence is calibrated, and whether silence or abstention is returned at low confidence. A high-probability display alone is not safe interpretation.
  • Long-term operation: not just within-session speed, but also tail latency, cross-day stability, and recalibration burden. A fast demo is not the same as a deployable loop.

One more front-door error had to be blocked here: papers that output fluent sentences can still be solving different problems at the task-design level. Rybár et al. (2024) showed that cue-period data can create apparently strong semantic BCI performance that does not survive into the separated mental-task window. Horikawa (2025) showed descriptive caption generation from viewed or recalled video content through semantic-feature decoding and iterative text optimization. Those are real advances, but they do not sit on one monotonic `brain-to-text` ladder with known-onset word decoding, prompt-conditioned language continuation, or invasive speech communication.

The front door was still too coarse when it let invasive language BCIs sound like one continuous success story. Willett et al. (2023) strengthened the same-session throughput route and also showed a bounded no-new-day-training slice (30% word error rate offline without new-day retraining), but the authors still said clinically viable multi-day adaptation remained unfinished. Littlejohn et al. (2025) strengthened streaming throughput / expressivity. Wairagkar et al. (2025) strengthened instantaneous voice synthesis with silence fallback, but even its session-1 decoder used same-day training. Singh et al. (2025) instead strengthened a cross-subject transfer / initialization route, and Karpowicz et al. (2025) plus Wilson et al. (2025) strengthened adaptive stabilization / unsupervised rescue. Those are different operational achievements, so general scalp EEG or ordinary non-invasive BCI cannot claim the same level without naming which route actually improved.

Q. If the score is high or cross-day stable, did we read the target neural variable?

A. Not necessarily. A score can stay high because the model is using shortcut routes rather than the intended neural variable. In EEG/BCI work, those routes can include eye position, facial/jaw/neck EMG, uninstructed movement, auditory feedback, subject / session fingerprint, and acquisition-distribution cues such as site, device, reference system, electrode layout, and protocol.

Musall et al. (2019) showed that trial-by-trial neural dynamics can be dominated by richly varied movements, Mostert et al. (2018) showed that visual-working-memory decode can retain an eye-movement confound, McFarland et al. (2005) showed that EMG can contribute to early BCI performance, Chaibub Neto et al. (2019) showed that repeated-measure record-wise splits can massively underestimate error through identity confounding, and Xu et al. (2020) showed that cross-dataset variability weakens EEG-decoding generalization.

At Mind-Upload, a result is not read as target-specific neural evidence unless the paper also fixes the target variable, nuisance-only baselines, slice-wise hold-out, and independence units for subject / session / acquisition distribution. The shortest follow-up is Verification: Specificity & Shortcut Card.

Q. If a foundation-model or leaderboard result is strong, did we solve general EEG decoding?

A. Not by default. On this site, a large EEG model or leaderboard result is first read as benchmark-conditioned transfer evidence, not as automatic proof that a general neural decoder already exists. The current literature already splits that evidence into at least four different objects. Jiang et al. (2024) already treated mismatched electrodes, unequal sample lengths, varied task designs, and low signal-to-noise ratio as core EEG-side barriers even while reporting LaBraM, and Lee et al. (2025) then found only marginal gains, about 0.5%, over conventional deep baselines despite much larger parameter counts. The newer setup-agnostic papers matter, but they matter in a narrower way: Han et al. (2025) target channel-permutation equivariance, Chen et al. (2025) target coordinate-based adaptation across heterogeneous devices and more than 150 layouts, and El Ouahidi et al. (2025) push setup-agnostic pretraining to more than 60,000 hours from 92 datasets and 25,000 subjects. Those are advances in recording-frame compatibility. They are still not proof that different montages, coordinate routes, and reference families already preserve one shared physiology-side representation. Ma et al. (2026) then show that strong EEG foundation models can still generalize poorly when subject-level supervision is limited unless extra adaptation structure is added, while Xiong et al. (2025), Liu et al. (2026), and Lahiri et al. (2026) show that protocol inconsistency, linear-probe versus fine-tuning regime, and pretraining-population diversity can materially change which checkpoint looks strongest.

One more front-door compression still remained: accepted conference papers, official benchmark-operation pages, and arXiv preprints could still be read as one evidence pile even though they answer different questions. The current source mix does not support that shortcut. On this site, Jiang et al. (2024) and Lee et al. (2025) are read as peer-reviewed route papers, the official EEG Challenge homepage, rules, submission page, and leaderboard are read as the current benchmark object and postmortem layer, and Han et al. (2025), Chen et al. (2025), El Ouahidi et al. (2025), Ma et al. (2026), Xiong et al. (2025), Liu et al. (2026), and Lahiri et al. (2026) are read as exploratory preprint routes or benchmark-warning analyses. That source-status split is now part of the front-door rule rather than background knowledge the reader has to infer.

If the source itself is... Safe reading on this site What it still cannot settle
peer-reviewed route paper Use it to say which route improved under a named task, transfer object, or adaptation regime. It still does not fix the current benchmark rules snapshot, organizer corrections, or field-wide ranking by itself.
official benchmark operations / postmortem Use it to define the executable benchmark object: current task mix, rules, disclosure burden, inference budget, and later organizer corrections. It still does not by itself explain the model-side mechanism or prove physiology-preserving transfer.
arXiv preprint / benchmark-warning paper Use it as exploratory evidence about setup tolerance, protocol fragility, scaling limits, or evaluation gaps that still need independent confirmation. It still does not by itself settle frontier rank, overturn the accepted route hierarchy, or replace an accepted benchmark rerun.

The phrase harmonized EEG is still too coarse for a front-door reading. The official EEG-BIDS specification already separates electrodes, channels, coordinate system, and reference scheme, while Hu et al. (2018) showed that reference montage and electrode setup alter the measured scalp potential itself and Dong et al. (2024) validated one explicit REST-based transformation route for cross-location harmonization. Inference from these sources: common-channel intersection, interpolation to a target montage, and REST-based transformation preserve different measurement objects. So when a paper says a model `works across setups`, this FAQ still asks which recording-frame branch was used before it lets the result sound like physiology-side equivalence.

If the paper directly advances... Representative sources What still must stop here
representation learning / efficiency Kostas et al. (2021), Jiang et al. (2024), Lee et al. (2025) Do not promote that result to a solved general decoder or a source-identifiable subject-invariant representation.
recording-frame compatibility Han et al. (2025), Chen et al. (2025), El Ouahidi et al. (2025) Do not treat layout tolerance or heterogeneous-device support as one shared physiology-preserving coordinate system.
label-limited adaptation rescue Lee et al. (2025), Ma et al. (2026) Do not say the pretrained model transferred without rescue, or that adaptation burden has disappeared from deployment.
benchmark governance / postmortem EEG Challenge (2025), Xiong et al. (2025), Liu et al. (2026), Lahiri et al. (2026) Do not read one leaderboard or benchmark paper as a stable field-wide capability ladder.

The benchmark object itself can also move. The official EEG Challenge (2025) homepage states that the proposal preprint is already out of date relative to execution-phase changes and that the current website plus Starter Kit should be treated as authoritative. The official data page shows that the benchmark family mixes six EEG tasks with psychopathology-factor prediction, while the official rules and submission page fix downsampled 100 Hz data, disclosure of extra pretraining corpora / pretrained checkpoints / fine-tuning method, a single-GPU 20 GB inference-stage constraint, and an inference-only code-submission regime. The final leaderboard then disclosed that Challenge 2 samples had not been randomized, allowing contiguous-trial same-subject structure to influence ranking and forcing separate awards. That means benchmark governance is not administrative detail; it changes what the score is allowed to mean.

At Mind-Upload, a foundation-model or leaderboard result is not promoted beyond qualified representation-learning / transfer evidence unless the paper also fixes pretraining corpus identity and overlap audit, benchmark object / supervision unit, coordinate route, reference family, omitted-channel policy, harmonization branch, adaptation regime or label budget, benchmark provenance / governance, and shortcut resistance against subject or setup fingerprints. The shortest follow-up is EEG 101, Verification: Pretraining Card, and Verification: Specificity & Shortcut Card.

If you want the site-wide reading rule for source type and status labels, continue to Wiki: How to read source types, status labels, and evidence classes.

Q. If BOLD or fNIRS changes, does that mean neural state changed?

A. Not automatically. Hemodynamic modalities carry both neural-side uncertainty and a vascular transfer state. So a group difference or longitudinal BOLD / HbO / HbR change can partly reflect baseline vascular state, cerebrovascular reactivity, or superficial/systemic contamination rather than a clean neural difference.

Murphy et al. (2011) showed that accounting for individual vascular reactivity improves group-level BOLD analyses, Williams et al. (2023) showed that task BOLD magnitude is strongly predicted by CVR across the cortex, Yücel et al. (2015) showed that short-separation regression is needed to reduce superficial confounds in fNIRS, and Epp et al. (2025) showed that significant task BOLD changes can coexist with opposite oxygen-metabolism changes in many voxels.

At Mind-Upload, a BOLD or fNIRS difference without vascular-state / CVR or short-separation audit stays a hemodynamic-limited difference rather than a clean neural difference. The shortest follow-up is Wiki: Observability and Claim Ceiling by Measurement Stack plus Verification: Observability Budget.

Q. If a paper shows EEG / MEG connectivity or information flow, did it identify communication channels or causality?

A. Not by default. On this site, sensor-space or source-space connectivity results are first read as dependence patterns under a named pipeline, not as leak-proof inter-areal communication maps or causal wiring. Vinck et al. (2011) made wPLI more conservative against some zero-lag mixing than older phase-synchrony measures, but that is not the same as eliminating leakage or proving directional influence.

The deeper problem is that the remaining failure modes are different from ordinary cleanup. Haufe et al. (2013) showed that sensor-space EEG connectivity remains strongly limited by volume conduction, Palva et al. (2018) showed that even leakage-insensitive source-space measures can generate ghost interactions, Ye et al. (2020) evaluated symbolic transfer entropy with TMS precisely because observational data alone make causality difficult to identify, and Miljevic et al. (2025) showed that sensor-space functional-connectivity estimates still change materially with rereferencing, epoch length, epoch count, and metric choice.

At Mind-Upload, a connectivity paper must therefore still disclose reference scheme and preprocessing route, leakage / volume-conduction countermeasures, source-model assumptions if used, perturbation or external validation route for directional claims, pipeline-sensitivity checks, and residual claim ceiling. If those are missing, we read the result as a pipeline-conditioned dependence map, not as a communication graph or causal circuit. The shortest follow-up is EEG 101, especially the connectivity-ceiling note, then Wiki: From observation to estimation.

Q. If a paper reports DCM or effective connectivity, did it find the brain's true causal wiring?

A. Not by default. On this site, DCM / effective-connectivity output is read as a model-conditioned causal hypothesis, not as automatic discovery of the one true circuit. Penny et al. (2004) showed that DCM conclusions are relative to the models being compared, and Rosa et al. (2012) showed that later workflows can search very large model spaces efficiently from one full model rather than make the true model unique. More recent scaling work such as Frässle et al. (2021) and Wu et al. (2024) pushes effective-connectivity estimation toward whole-brain or faster settings, but it still remains inside an explicitly chosen generative model and observation model.

That still leaves several failure modes open. Villaverde et al. (2019) showed that unknown inputs, states, and parameters often have to be assessed jointly, not one by one. Smith et al. (2011) showed that lag-based fMRI approaches perform poorly and that functionally inaccurate ROIs are extremely damaging to network estimation. Zhang et al. (2024) then showed that reasonable task-fMRI processing choices, especially GLM design and activation contrast, can materially alter group-averaged effective-connectivity patterns and parameter certainty. Barnett & Seth (2017) showed detectability black spots under subsampling, Vink et al. (2020) showed that resting-state EEG functional connectivity explains less than 10% of TMS-evoked propagation variance, Novelli et al. (2025) showed that slow BOLD sampling can still induce spurious Granger-causal inference even when realistic HRF variability alone need not do so, and Yan et al. (2026) showed that latent confounders remain an active challenge in biological network reconstruction.

That does not make effective-connectivity work useless. It means the safe claim is narrower: under a disclosed node set, omitted alternatives, observed-subsystem boundary, node-definition policy, processing / first-level design policy, prior family, and observation assumptions, one model family explained the data better than named competitors. Even reproducibility is conditional. Frässle et al. (2016), Jafarian et al. (2024), and Ma et al. (2024) show that effective-connectivity reliability can look strong under tightly matched task/rest, session-interval, scan-duration, and sample-size conditions, but that is still not the same as proving a unique causal circuit in the wild.

At Mind-Upload, a paper that says “effective connectivity” must therefore still disclose candidate model space, observed-subsystem closure / latent-confound audit, node-definition policy, processing / first-level design policy, sampling / transformation sensitivity, family comparison or model recovery, held-out perturbation / external validation, reliability window, and abstention boundary. If those are missing, we read it as a model-conditioned causal hypothesis, not as causal-wiring discovery. The shortest follow-up is Wiki: effective-connectivity route card, Verification: Observability Budget, and Roadmap R4.

Q. If a paper reports entropy production, irreversibility, or arrow-of-time in brain data, did it measure the brain's physical dissipation or WBE-ready thermodynamic cost?

A. Not by default. On this site, thermodynamic language is split before interpretation. Bérut et al. (2012) tested the Landauer lower bound for bit erasure, Attwell & Laughlin (2001) summarized tissue-side signaling costs, and papers such as Lynn et al. (2021) and Ishihara & Shimazaki (2025) estimate nonequilibrium quantities from neural data. Those objects are related, but they are not the same measurement.

In the current primary literature, the same thermodynamic vocabulary still hides different estimator families. Lynn et al. (2021) estimated entropy-production lower bounds from coarse-grained BOLD state transitions, Deco et al. (2022) used time-shifted correlation asymmetry, de la Fuente et al. (2023) used inversion decoding on ECoG, Nartallo-Kaluarachchi et al. (2025) used directed visibility graphs on MEG, and Ishihara & Shimazaki (2025) estimated model-based entropy flow under a state-space kinetic Ising model. So the phrase thermodynamic result does not by itself tell you whether the paper reported a lower bound, an asymmetry score, a graph index, or a model-based flow estimate.

Just naming the estimator family is still too weak. Lynn et al. (2021) showed that the estimate depends on how macrostates are coarse-grained, de la Fuente et al. (2023) showed that reversibility detection depends on principal-component choice, input features, and model complexity, Martínez et al. (2019) showed that waiting-time asymmetry can reveal hidden dissipation even when observable current vanishes, Blom et al. (2024) showed that coarse lumping can hide dissipative cycles and introduce memory so that entropy-production estimates become far too small when the observed trajectory is naively treated as Markov, Ishihara & Shimazaki (2025) explicitly notes that pairwise and conditional-independence assumptions limit interpretation and uses trial-shuffled controls to separate coupling-related contributions, and Baiesi et al. (2024) showed that sparse or unobserved reverse transitions can break direct entropy-production estimation even when the analysis otherwise looks clean. The next weakness is operational rather than mathematical. Poudel et al. (2024) showed that small motion can materially alter visibility-graph structure and that only low-motion subsets reached moderate-to-high test-retest reliability for selected metrics, Metzen et al. (2024) showed that BOLD variability and complexity measures have markedly different reliability profiles, and Chen et al. (2025) showed with simultaneous EEG-PET-MRI that temporal coupling across modalities can coexist with non-identical spatial organization and state trajectories. At Mind-Upload, such a paper must therefore disclose signal route and state definition, coarse-graining / timescale, observed-state closure / hidden-degree risk, estimator family and dynamical assumptions, null / surrogate control, stability / nuisance sensitivity, cross-estimator concordance if the claim is strengthened, reverse-transition support / finite-data handling, quantity type, physiology-side grounding and bridge quality if energetic language is used, cost isolation, and abstention boundary. If those are missing, we keep the result at the level of an exploratory auxiliary analysis, not a direct readout of microscopic dissipation, metabolic cost, or WBE-relevant validity. The shortest follow-up is Wiki: irreversibility route card plus Verification: thermodynamic indicators.

Q. What is the difference between decode and emulate?

A. Decode means translating observations. Emulate means having an internal state that evolves over time, responds to intervention, and generates outputs. To move closer to WBE, the benchmark has to evaluate the second kind of claim, not only the first.

Recent non-invasive word decoding and streaming speech neuroprostheses are major advances as communication routes. But at Mind-Upload, we do not read them as emulation, let alone as WBE evidence, unless the work also establishes neural contribution beyond language prior, OOD and cross-day generalization, matching after intervention, tail latency, silence, and recalibration burden, and auditing of hidden state. What has advanced first is decode, or at most local subsystem closed loop.

WBE 101, the Glossary, and Wiki: Decode vs. Emulate are the shortest follow-up route.

Q. If an LLM or digital twin talks like a person, is that Mind-Upload?

A. Not by itself. Natural conversation could reflect imitation of outward behavior, or it could reflect continuity of internal state and causal structure. Those are different questions.

Mind-Upload cares not only about whether something looks human-like, but whether the responses under changed conditions, the continuity of memory and learning, and the response to falsification conditions are all disclosed. Natural appearance matters as a clue, but it is not enough to move to an L4 identity claim.

Wiki: Counterfactual, intervention, and perturbation verification explains in stages why “it can talk naturally” is not enough.

Q. If we know the connectome and cell type, is the rest mostly filled in?

A. Not yet. Wiring and cell type still leave broad families of state latent. Gouwens et al. (2021) showed morpho-electric spread even within the same transcriptomic type, Grubb & Burrone (2010) showed activity-dependent AIS relocation that retunes excitability, Santoni et al. (2024) showed that chromatin plasticity can predetermine neuronal eligibility for memory trace formation, and Wang et al. (2015), Dai et al. (2019), Shi et al. (2018), Peterson et al. (2025), and Li et al. (2025) show that post-transcriptional RNA-state is not one row: Wang et al. (2015) is a splice-isoform route whose downstream object is chromatin / transcriptional control, Dai et al. (2019) is a splice-dependent transsynaptic receptor-balance route, Shi et al. (2018) and Li et al. (2025) are different m6A translation-versus-degradation routes, and Peterson et al. (2025) is an RNA-editing route for homeostatic AMPAR composition. Therefore, even when gene-level abundance looks similar, the operative RNA controller can still differ across memory-relevant mechanism families. Giese et al. (1998), Lee et al. (2003), Rodrigues et al. (2004), Tomita et al. (2005), and Vierra et al. (2023) show that phospho-signaling / second-messenger state is another layer: phosphosite occupancy and signaling nanodomains can still change plasticity expression even when transcript or bulk protein abundance looks similar. Govindarajan et al. (2011) showed branch-level protein-synthesis-dependent LTP integration, Park et al. (2006), Zhao et al. (2020), and Swarnkar et al. (2021) showed that compartment-specific cargo delivery is another state layer for spine growth, synaptic plasticity, and memory, Frischknecht et al. (2009) showed that ECM constrains AMPA-receptor mobility and short-term plasticity, Glykys et al. (2014) showed that local impermeant anions constrain neuronal chloride concentration, and Seidl et al. (2015) showed that node and internode geometry can tune conduction timing.

If by “connectome” one means a human diffusion-MRI tractography connectome, the object is even coarser than the word suggests, and it is not even one stable graph by default. Thomas et al. (2014) found no high-anatomical-accuracy solution across tractography methods even with exceptional ex vivo macaque diffusion data, Reveley et al. (2015) showed that superficial white matter can block long-range tracking from large parts of cortex, Donahue et al. (2016) found useful but incomplete prediction of tracer-weighted corticocortical connectivity, Schilling et al. (2020) showed that high accuracy mainly appears when strong anatomical start / end / exclusion priors are supplied, and Grisot et al. (2021) localized recurring same-brain errors at branching and turning configurations. Newer route-audit work tightened the ceiling further: Gajwani et al. (2023) showed that hub location and node strength can vary strongly across tractography pipelines and parcellations, He et al. (2024) showed that tractogram filtering can shift laterality indices for more than 10% of connections, McMaster et al. (2025) showed that voxel-size variance changes the resulting connectome, Bramati et al. (2026) showed on the same 3 T scanner with uniform processing that diffusion-sampling scheme alone still shifts voxel metrics and tractography outputs, Manzano-Patrón et al. (2025) made fibre-orientation uncertainty explicit instead of silent, and Zhu et al. (2025) improved reconstruction only by adding microscopy to MRI rather than by assuming MRI alone had already fixed the graph. At Mind-Upload, a tractography-derived human connectome is therefore read as an acquisition-, endpoint-, graph-construction-, and uncertainty-conditioned macro pathway prior or bundle-level hypothesis, not as an edge-complete human connectome. The longer rule is in Wiki: tractography route card and Verification: Observability Budget.

Likewise, Hengen et al. (2016), Torrado Pacheco et al. (2021), and Xu et al. (2024) show that sleep-dependent homeostasis and network recovery remain additional variables. Gibson et al. (2014), McKenzie et al. (2014), and Looser et al. (2024) show that myelin and oligodendrocyte support affect timing and axonal health. Separately, Hardingham & Larkman (1998), Volgushev et al. (2000), Moser et al. (1993), and Long & Fee (2008) show that local thermal-state can change synaptic reliability, spike generation, field-potential amplitude, and sequence timing even without rewiring. The human lane is already split further: healthy-human MRS thermometry (Rzechorzek et al., 2022), task-linked thermal mapping (Rogala et al., 2024), and frontal-lobe thermometry (Tan et al., 2025) remain passive or task-linked macro thermal proxies, while Tan et al. (2024) and Inoue et al. (2025) add bounded human perturbation-conditioned thermal routes through severe heat exposure and intraoperative focal cooling. None of those human rows, however, is cell-specific thermal ground truth. Separately, Rangaraju et al. (2014), Rangaraju et al. (2019), Divakaruni et al. (2018), Bapat et al. (2024), and Hu et al. (2025) show that local ATP supply, mitochondrial positioning, fission/fusion, and synaptic ATP-synthase organization remain additional hidden state for repeated-burst reliability and dendritic plasticity. Current human energetic routes now have to be split more narrowly: Ren et al. (2015) is a 31P metabolite / pH balance route, Ren et al. (2017) is a 31P MT exchange-flux route, Guo et al. (2024) is a whole-brain NAD-content route, Kaiser et al. (2026) is a functionally localized NAD-dynamics route, Karkouri et al. (2026) is a deuterium metabolite-mapping / absolute-quantification route, and Li et al. (2025) is a deuterium kinetic-rate route. Those human advances are real, but they are still macro energetic proxies rather than branch-local mitochondrial readouts, and they are not interchangeable with one another. The same human ceiling applies to post-transcriptional RNA-state: current in vivo routes and ordinary short-read transcript summaries do not directly reveal isoform choice, m6A reader engagement, or RNA-editing ratios across the whole living human brain, while specialized long-read atlas work such as Joglekar et al. (2024) remains a targeted ex vivo / atlas-building route rather than a whole-brain in vivo readout. The same human ceiling also applies to phospho-signaling / second-messenger state: current in vivo routes do not directly reveal phosphosite occupancy, kinase/phosphatase balance, or compartment-specific signaling nanodomains across the living whole human brain, while ex vivo phosphoproteome atlas work such as Biswas et al. (2023) remains an atlas route rather than a living whole-brain readout. The same human ceiling also applies to cargo routing: current in vivo routes do not directly reveal branch-specific motor engagement, cargo pausing, or bouton-level retention. Likewise, human sodium MRI routes such as Qian et al. (2012) and Qian et al. (2025) are important macro ionic proxies, but they still do not directly reveal cell-specific chloride concentration, KCC2 / NKCC1 balance, or local EGABA. The same split now applies to glial metabolism / substrate routing: Suzuki et al. (2011) is a lactate-shuttle route, Silva et al. (2022) is a starvation ketone-body route, Pavlowsky et al. (2025) is an intensive-learning glia-to-neuron fatty-acid route, and Greda et al. (2025) is an apoE / sortilin-dependent lipid-delivery and fuel-choice route. These papers do not share one fuel object, one supplier cell, one neuronal sink, one regime trigger, or one human observability ceiling, so this site does not treat `glial support` as one solved row. Astrocyte-state then stays separate again from glial fuel routing: Cahill et al. (2024), Williamson et al. (2025), Dewa et al. (2025), and Bukalo et al. (2026) show local transmitter encoding, recall, multiday stabilization, and fear-state representation routes, while human astrocyte PET routes such as Villemagne et al. (2022), Tyacke et al. (2018), and Livingston et al. (2022) remain target-defined proxy families rather than local controller readouts. On this site, those rows raise the need to keep both glial substrate-routing and astrocyte-state explicit, but they still do not permit a jump to direct human whole-brain memory readout.

The same bucket is too coarse for sleep architecture / replay-coupling. Ngo et al. (2013) showed that auditory stimulation benefits memory only under a phase-locked slow-oscillation policy, Baxter et al. (2023) showed that closed-loop stimulation can alter SO / spindle dynamics while still failing to improve memory if sleep continuity is disturbed, Whitmore et al. (2022) showed that TMR benefit depends on ample and undisturbed N3 sleep, Schreiner et al. (2021) constrained endogenous scalp-EEG decoding around aggregated slow-oscillation / spindle events, Schreiner et al. (2023) showed that respiration-linked SO-spindle coupling is related to reactivation strength, Geva-Sagiv et al. (2023) showed that an intracranial closed-loop synchrony intervention improves human overnight memory only when precisely time-locked, Schreiner et al. (2024) linked spindle-locked ripples to human memory reactivation, Whitmore et al. (2024) showed that sleep-disruption effects depend on memory age, Jourde et al. (2025) showed that the effectiveness of auditory stimulation depends on thalamocortical spindle phase, Duan et al. (2025) showed that one human TMR session can contain both strengthening and decaying items, Shin et al. (2025) showed that behavioral benefit can concentrate in challenging memories rather than across all items, and Deng et al. (2025) showed that even within NREM the consolidation window is time-structured. At Mind-Upload, that means sleep happened, oscillations increased, a cue was delivered, overnight memory changed, and replay-coupling matched are not treated as interchangeable statements. The route has to log sleep-integrity burden, NREM physiology gating, and memory age / selection regime in addition to timing. The longer rule is in Wiki: sleep replay route card and Verification: maintenance-state error budget.

The same correction also applies to neurovascular-unit / BBB / pericyte state. Bell et al. (2010) showed that adult pericyte loss produces hypoperfusion, BBB breakdown, and later memory impairment, Kisler et al. (2020) showed rapid neurovascular uncoupling after acute pericyte ablation, Pandey et al. (2023) showed that pericyte-derived IGF2 is required for long-term memory, Swissa et al. (2024) linked cortical plasticity to BBB modulation, and Mai-Morente et al. (2025) showed that a pericyte capillary-diameter controller affects memory. Current human BBB routes such as Padrela et al. (2025) and Morgan et al. (2024) constrain water exchange, while Chung et al. (2025) constrains tracer-specific BBB transport. A distinct human blood-CSF-barrier lane also exists, and it is not one internal quantity either: Zhao et al. (2020) and Sun et al. (2024) constrain choroid-plexus perfusion, Petitclerc et al. (2021) constrains blood-to-CSF water transport, Anderson et al. (2022) constrains choroid-plexus water cycling, Wu et al. (2026) constrains apparent BCSFB exchange, and Petitclerc et al. (2026) constrains joint BBB-versus-BCSFB ASL exchange in one acquisition. Those are still bounded human support-state routes rather than direct readouts of the responsible pericyte, endothelial, or choroid-plexus epithelial controller. At Mind-Upload, this layer is therefore kept separate both from measurement-side vascular-state / CVR audit and from clearance / immune support.

The same correction applies to shared extracellular / electrical state. Galarreta & Hestrin (1999) showed that fast-spiking interneurons can form electrical-synapse networks, Anastassiou et al. (2011) showed that endogenous extracellular fields can causally bias cortical spike timing, Burman et al. (2023) showed that active cortical networks can shift fast inhibition toward a predominantly shunting regime in vivo, Yang et al. (2024) showed that activity-dependent electrical synapses can rewire local networks for persistent oscillations, and Selfe et al. (2024) showed that direct inhibitory driving-force measurement requires a specialized local optical route. Human evidence is route-split even before any strong reading: Feld et al. (2026) is useful as a perturbation-conditioned clue that electrical coupling can matter for spindle-to-slow-oscillation coordination during sleep, but it is still not a direct whole-brain readout of local electrical state. At Mind-Upload, a chemical connectome plus nominal inhibitory edges is therefore not read as electrical-state complete. If a paper mixes these routes, this site now asks for an electrical-state route card that names claim family, direct observable, spatial regime, perturbation / calibration route, human evidence class, and abstention.

The same bucket was also too coarse for extracellular-space geometry / diffusion-barrier / osmotic-regime routes. Graydon et al. (2014) showed that synapse-adjacent morphology changes extracellular dilution and signaling, Kilb et al. (2006) and Lauderdale et al. (2015) showed that osmotic ECS contraction / edema can rapidly increase excitability, Xie et al. (2013) showed sleep-linked interstitial-space expansion in mice, Voldsbekk et al. (2020) gave a bounded human diffusion-MRI clue consistent with wakefulness-related extra-axonal / extracellular-volume reduction, and Örzsik et al. (2023) added a sleep-conditioned higher-order diffusion / glymphatic clue under a within-subject sleep-deprivation-plus-zolpidem regime. Therefore, at Mind-Upload a chemical connectome plus nominal inhibitory edges is not read as extracellular-state complete either.

At Mind-Upload, this means we treat connectome-complete as progress on the structural scaffold, not as emulation-complete. Current excitability, timing-state, thermal-state, transcription/chromatin, post-transcriptional RNA-state, local proteostasis, cargo-transport / cytoskeletal trafficking state, ECM / PNN gate, ionic milieu, bioenergetic / mitochondrial state, neurovascular-unit / BBB / pericyte state, sleep/controller state, glial substrate-routing, astrocyte-state, and clearance / immune support still need to be disclosed or left explicitly latent. So same-day activity matching, cross-day stability, and maintenance-consistent dynamics remain separate claims. The shortest follow-up is Wiki: Why wiring diagrams alone are not enough plus Wiki: Homeostatic plasticity and maintenance state.

The same correction applies to clearance / immune support. Louveau et al. (2015) and Ahn et al. (2019) established meningeal-lymphatic drainage routes, Kim et al. (2025) showed that the meningeal-lymphatics-microglia axis can regulate synaptic physiology, and the human lane is no longer transport-only. Biechele et al. (2023) showed why TSPO is not a universal human activation-state meter, Wijesinghe et al. (2025) validated TSPO PET as a microglial biomarker in PSP, Horti et al. (2022) plus Ogata et al. (2025) established first-in-human CSF1R PET routes, and Yan et al. (2025) quantified COX-2 in healthy human brain. Fultz et al. (2019) then showed a macroscopic sleep-linked CSF-oscillation route, Kim, Huang, & Liu (2025) showed a parenchyma-CSF water-exchange route, Lim et al. (2025) showed an awake-state respiration-conditioned CSF net-flow route, Yoo et al. (2025) showed an exercise-conditioned contrast-influx / meningeal-lymphatic-flow route, Eide et al. (2023) showed an intrathecal tracer / CSF-to-blood clearance-capacity route, Hirschler et al. (2025) showed a CSF-mobility route, and Dagum et al. (2026) showed a model-based sleep-linked biomarker-efflux route. On this site, that means clearance is not treated as passive cleanup, but current human evidence is read as two bounded lanes, macro support-state transport proxy and target-defined neuroimmune PET, not as direct identification of a local immune controller or synapse-specific maintenance mechanism.

The separate question of what human measurement can actually observe today is handled in Q2d. That separation is deliberate: connectome insufficiency and human observability ladder are related, but they are not the same reading task.

Q. If same-brain functional connectomics or a digital twin works, did we solve a local twin?

A. Not yet. Bosch et al. (2022) showed that linking live physiology to later ultrastructure already requires a multistage landmark-based bridge, and MICrONS Consortium et al. (2025) strengthened that route to a same-brain local dataset with about 75,000 neurons linked to a later EM reconstruction of more than 200,000 cells and 0.5 billion synapses. That is a major advance in same-brain local structure-function linkage, but it is still a sequential local pipeline, not a simultaneous whole-state sample. Ding et al. (2025) then added a validated stimulus-conditioned response model, while also warning that the model's internal representations still need cautious interpretation. Gamlin et al. (2025) sharpened the cell-type bridge, but still through morphology-based predicted transcriptomic labels rather than direct transcriptomic assay inside the EM volume.

The remaining ceiling is not cosmetic. Holler et al. (2021) showed that inferring function from wiring diagrams is limited by unresolved synaptic-strength structure, Molnár et al. (2016) showed that human synapses can contain multiple docked vesicles and multivesicular release, Sakamoto et al. (2018) showed that Munc13-1 supramolecular assemblies set independent release sites, Dürst et al. (2022) showed that vesicular release probability strongly sets synaptic strength, Emperador-Melero et al. (2024) showed that CaV2 clustering and vesicle priming are executed by distinct active-zone machineries, and Mittermaier et al. (2024) showed that membrane-potential state gates synaptic consolidation in human neocortical tissue. Beiran & Litwin-Kumar (2025) then showed that connectome-constrained recurrent networks can still remain dynamically degenerate until additional recordings narrow the compatible family. So at Mind-Upload the safe ceiling is a sequential local structure-function scaffold plus, at most, a task-bounded conditional predictor. It is not direct transcriptomic truth, not a readout of release-site number, docked-vesicle architecture, active-zone nanostructure / priming-site assembly, or current release competence, and not one solved local twin. The shortest follow-up is Wiki: Why a Connectome Is Not Enough, Wiki: Observability and Claim Ceiling by Measurement Stack, Wiki: State-Continuity Bridge, and Wiki: Decode vs. Emulate.

Q. If human measurement keeps improving, are we close to state-complete readout?

A. Not yet. The first split is between destructive local ex vivo structure and living-human in vivo proxy routes. The second split is inside the human routes themselves: recent human advances do not all report the same quantity. Lu et al. (2023) showed why preservation route changes extracellular-space retention and native geometry, and Shapson-Coe et al. (2024) reconstructed a cubic millimeter of human temporal cortex at nanoscale resolution, but as a rapidly preserved local surgical fragment, not a living whole-brain state readout. By contrast, Johansen et al. (2024) built an SV2A PET atlas in healthy humans (17F/16M) calibrated with postmortem autoradiography, which is a regional synaptic-density proxy. Smart et al. (2021) showed that brief visual activation does not measurably change [11C]UCB-J binding, and Holmes et al. (2022) found no measurable overall SV2A change 24 h after ketamine despite symptom improvement, so even a strong SV2A PET route remains a regional density proxy rather than a momentary release-machinery readout. Lucchetti et al. (2025) used five-metabolite 1H-MRSI in 51 healthy participants with an independent replication sample of 13 to derive a parcel-level biochemical similarity scaffold, while Guo et al. (2025) used ultrahigh-field extended spatiospectral encoding plus subspace modeling to produce high-resolution 1H-MRSI metabolite-distribution maps under explicit ghosting / aliasing / low-SNR handling. The spectroscopy rows already split further: Ren et al. (2015) reported resting ATP synthesis, phosphorus-metabolite concentrations, pH, and T1 in 12 resting subjects; Ren et al. (2017) estimated PCr→ATP and Pi→ATP exchange fluxes from a 5-pool magnetization-transfer model in six resting subjects; Guo et al. (2024) mapped whole-brain intracellular NAD content at 2.3 cc nominal resolution with a 1.0 cc feasibility dataset; Kaiser et al. (2026) used prior fMRI to localize a visual-cortex voxel and reported task-evoked NAD+ dynamics in 25 healthy volunteers; Karkouri et al. (2026) used a dedicated absolute-quantification pipeline at 7 T to produce HDO / Glc / Glx / Lac maps and associated rate estimates in a mixed cohort of 12 healthy volunteers and 5 treatment-naive glioblastoma patients, with only two healthy volunteers studied after [6,6'-2H2]glucose; Li et al. (2025) estimated glucose-transport and metabolic-rate maps using 7 T dynamic DMRSI, blood-input / kinetic modeling, and 0.7 cc nominal voxels in five healthy participants; Ahmadian et al. (2025) showed that [6,6'-2H2]glucose dose materially changes human brain-side deuterated-glucose and Glx visibility; and Bøgh et al. (2024) showed that repeatability at 3 T depends on a named acquisition and time-point regime. van Blooijs et al. (2023) estimated tract-scale transmission speed in a developmental human route, which is a timing-support advance but not a myelin-specific MRI quantity. Baadsvik et al. (2024) demonstrated myelin-bilayer mapping in two healthy volunteers. Morgan et al. (2024) showed that even BBB water-exchange estimates differ materially across ASL route choices, while Chung et al. (2025) quantified tracer-specific BBB permeability-surface-area product with dynamic PET and kinetic modeling, but also stated that human ground truth and test-retest validation remain future work. A distinct human blood-CSF-barrier lane also exists: Zhao et al. (2020) measured choroid-plexus perfusion, Sun et al. (2024) extended that perfusion lane with a 641-person HCP-Aging analysis, Petitclerc et al. (2021) measured blood-to-CSF water transport, Anderson et al. (2022) estimated choroid-plexus water cycling, Wu et al. (2026) reported apparent BCSFB exchange with scan-rescan repeatability, and Petitclerc et al. (2026) jointly estimated BBB-versus-BCSFB ASL exchange in one acquisition. Villemagne et al. (2022) and Tyacke et al. (2018) then showed that human astrocyte-related PET already splits into MAO-B and I2BS target classes rather than one generic astrocyte scalar. Finally, Fultz et al. (2019) showed macroscopic NREM-linked CSF oscillations, Kim, Huang, & Liu (2025) showed parenchyma-CSF water exchange in healthy humans, Eide et al. (2023) linked intrathecal gadobutrol retention and PK-based CSF-to-blood clearance variables to plasma biomarkers in neurological patients, Hirschler et al. (2025) showed whole-brain rest CSF-mobility maps in 20 analyzed healthy younger individuals together with a separate CAA comparison cohort, and Dagum et al. (2026) advanced sleep-linked biomarker efflux through an investigational device plus multicompartment model in a multi-site randomized crossover study whose primary analysis included 39 participants.

Human route What it directly strengthens What it still does not give you
Destructive local ultrastructure
Lu et al. (2023); Shapson-Coe et al. (2024)
A local human structural scaffold at nanoscale resolution, with explicit preservation-route dependence. A living whole-brain readout of current state, maintenance-state, longitudinal dynamics, or native-state preservation by default.
SV2A PET atlas
Johansen et al. (2024)
A regional synaptic-density proxy calibrated against postmortem autoradiography. Momentary synaptic efficacy, release-site number, docked-vesicle architecture, active-zone nanostructure / priming-site assembly, current release competence, branch-local plasticity state, or current individual whole-brain state closure.
Five-metabolite 1H-MRSI similarity scaffold
Lucchetti et al. (2025)
A parcel-level biochemical similarity object built from five metabolites. A flux map, a wiring graph, or current transcription / chromatin / post-transcriptional / phospho-signaling / proteostasis control.
High-resolution 1H-MRSI metabolite-distribution mapping
Guo et al. (2025)
A high-resolution ultrahigh-field metabolite-distribution route with explicit reconstruction and artifact-handling burden. A parcel-similarity scaffold, a deuterium absolute-quantification route, a kinetic-rate map, or current transcription / chromatin / post-transcriptional / phospho-signaling / proteostasis control.
31P-MRS metabolite / pH balance route
Ren et al. (2015)
A human metabolite / pH balance route for ATP synthesis, phosphorus-metabolite concentrations, pH, and relaxation behavior. Parcel-to-parcel biochemical similarity, model-conditioned exchange flux, whole-brain NAD content, localized task-evoked NAD dynamics, branch-local mitochondrial positioning, or local ATP-reserve control.
31P MT exchange-flux route
Ren et al. (2017)
A model-based route for PCr→ATP and Pi→ATP exchange-flux estimation at 7 T. Whole-brain NAD maps, localized task-evoked NAD dynamics, parcel-similarity structure, or direct mitochondrial-controller identity.
31P NAD-content mapping
Guo et al. (2024)
A whole-brain intracellular NAD-content map at 7 T with repeat-scan reproducibility. Task-evoked local NAD dynamics, route-independent energetic balance, branch-local reserve, or controller identity.
Localized functional 31P NAD-dynamics
Kaiser et al. (2026)
A functionally localized visual-cortex route for task-evoked NAD+ dynamics. A whole-brain NAD map, route-free energetic-balance readout, or task-general hidden-state closure.
Deuterium metabolite-mapping / absolute quantification
Karkouri et al. (2026)
Absolute HDO / Glc / Glx / Lac maps from a named 7 T deuterium quantification pipeline. Equivalence to the 31P routes above, route-free kinetic-rate interpretation, generic dose invariance, or direct mitochondrial-controller identity.
Dynamic deuterium kinetic-rate imaging
Li et al. (2025)
Macro glucose-transport and metabolic-rate maps from a specialized deuterium route with blood-input and kinetic modeling. Absolute metabolite distributions without route-specific quantification assumptions, equivalence to the 31P routes above, a direct mitochondrial-controller readout, or same-subject whole-brain hidden-state closure.
Human tract-scale transmission-speed estimation
van Blooijs et al. (2023)
A tract-scale timing-support estimate in living humans. A myelin-specific MRI quantity, axon-specific conduction-state ground truth, or whole-brain maintenance-state closure.
Myelin-bilayer mapping
Baadsvik et al. (2024)
A quantity-defined myelin-bilayer proof-of-principle from a highly specialized human MRI route. An interchangeable all-purpose myelin meter, axon-specific conduction-state ground truth, or whole-brain maintenance-state closure.
BBB water-exchange routes
Morgan et al. (2024); Padrela et al. (2025)
Human BBB water-exchange estimates under named ASL routes with method- and model-dependent burdens. A tracer-specific transport estimate, a generic BBB leakiness scalar, the responsible pericyte / endothelial controller, or a direct local maintenance-state readout.
Tracer-specific BBB transport route
Chung et al. (2025)
Tracer-specific BBB permeability-surface-area estimates under high-temporal-resolution dynamic PET and kinetic modeling. A route-independent BBB scalar, blood-CSF-barrier transport, or the responsible pericyte / endothelial controller.
Blood-CSF barrier / choroid-plexus perfusion / transport / water-cycling / apparent-exchange routes
Zhao et al. (2020); Sun et al. (2024); Petitclerc et al. (2021, 2026); Anderson et al. (2022); Wu et al. (2026)
Choroid-plexus perfusion, blood-to-CSF water transport, DCE water cycling, apparent BCSFB exchange, or joint BBB-versus-BCSFB ASL exchange under route-specific models. A generic BBB scalar, a generic clearance truth, the responsible choroid-plexus epithelial transporter state, or a route-free local maintenance-state readout.
Paired CSF-plasma protein-balance proteomics route
Farinas et al. (2025)
Paired-fluid CSF/plasma protein ratios across 2,304 proteins in 2,171 healthy or cognitively impaired older individuals under one proteomic assay family. A generic BBB or BCSFB permeability scalar, absolute concentration truth, the responsible transporter identity, or route-free local maintenance-state readout.
SMBT-1 MAO-B target-validation route
Villemagne et al. (2022)
A selective living-human MAO-B brain route with pharmacological blockade, reversible kinetics, and first-in-human target-validation logic. An AD-context contrast, a quantification-method paper, a whole-body tracer-burden route, or a generic astrocyte-state scalar.
SMBT-1 AD-spectrum disease-context route
Villemagne et al. (2022)
A pathology-context brain route showing higher regional SMBT-1 binding across the AD continuum and association with Aβ burden. A route-free MAO-B baseline, a quantification-method paper, or a substitute for first-in-human target validation.
SMBT-1 brain-quantification route
Hiraoka et al. (2025)
A named brain quantification route whose reading depends on arterial sampling, compartment-model comparison, and reference-region choice. A route-free disease readout, whole-body tracer burden, or a generic astrocyte-state meter.
SL25.1188 MAO-B disease / severity routes
Matsuoka et al. (2026); Best et al. (2026)
A separate MAO-B tracer family whose reading depends on simplified-versus-kinetic quantification in AD or on severity and smoking covariates in AUD. An SMBT-1-equivalent route family, an I2BS route, a route-free astrocyte scalar, or a direct local astrocyte-controller readout.
I2BS brain astrocyte PET route
Tyacke et al. (2018); Livingston et al. (2022)
A different target class for astrocyte-related PET whose disease-context interpretation can vary with region and impairment stage. An MAO-B-equivalent tracer family, a route-free astrocyte scalar, or a direct local astrocyte-controller readout.
Whole-body SMBT-1 biodistribution
Mesfin et al. (2026)
A tracer-burden route showing organ uptake, hepatobiliary / intestinal excretion, and whole-body distribution constraints for SMBT-1 in healthy humans. A brain astrogliosis map, an AD-context disease readout, or a substitute for brain quantification choices.
Macroscopic sleep-linked CSF oscillation
Fultz et al. (2019)
Sleep-state coupling among electrophysiology, hemodynamics, and large-scale CSF oscillation. Direct solute flux, segment-resolved drainage assignment, or local immune-controller identity.
Parenchyma-CSF water exchange
Kim, Huang, & Liu (2025)
An MT spin-labeling route for parenchyma-CSF water exchange with age-associated change in healthy humans. Protein-clearance capacity, intrathecal tracer clearance, or route-free glymphatic truth.
Respiration-conditioned CSF net flow
Lim et al. (2025)
An awake-state route for plane-specific CSF net flow enhanced by respiration. Natural-sleep baseline clearance capacity, route-free glymphatic truth, or segment-resolved lymphatic identity.
Exercise-conditioned contrast influx / meningeal-lymphatic flow
Yoo et al. (2025)
An intravenous-contrast-derived route for putative glymphatic influx and parasagittal meningeal-lymphatic flow after long-term exercise. An endogenous baseline transport meter, route-free glymphatic truth, or local immune-controller identity.
Intrathecal tracer / CSF-to-blood clearance route
Eide et al. (2023)
A PK-modeled intrathecal gadobutrol retention and CSF-to-blood clearance-capacity route linked to plasma biomarkers. Natural-sleep whole-brain flux ground truth, route-free glymphatic truth, or segment-resolved lymphatic identity.
CSF-mobility MRI route
Hirschler et al. (2025)
Whole-brain CSF-mobility structure with region-specific physiological drivers. Direct molecular flux, tracer clearance capacity, or local immune-controller identity.
Sleep-linked biomarker-efflux model
Dagum et al. (2026)
Model-based overnight amyloid-beta / tau efflux to plasma under randomized crossover sleep manipulation. A route-free glymphatic scalar, segment-resolved transport map, or cell-specific controller readout.
Human astrocyte PET needs a route-role split inside the tracer family

Separating MAO-B from I2BS is necessary, but it is no longer sufficient. Within the SMBT-1 MAO-B family alone, Villemagne et al. (2022) is a first-in-human target-validation paper, Villemagne et al. (2022) is an AD-spectrum disease-context paper, Hiraoka et al. (2025) is a brain quantification paper, and Mesfin et al. (2026) is a whole-body biodistribution paper. Within the separate SL25.1188 MAO-B family, Matsuoka et al. (2026) is a simplified / arterial-free AD quantification paper and Best et al. (2026) is an AUD severity / smoking-conditioned disease paper. Therefore, saying only MAO-B PET is still too coarse: this site now asks for the target, the tracer family, the route role, the quantification route, and the cohort / covariate regime.

Human clearance-transport also needs a family split at the FAQ front door

The same correction now applies inside human clearance-support routes. Fultz et al. (2019) is a macroscopic sleep-linked CSF-oscillation route, Kim, Huang, & Liu (2025) is a parenchyma-CSF water-exchange route, Lim et al. (2025) is a respiration-conditioned net-flow route, Yoo et al. (2025) is an exercise-conditioned contrast-influx / meningeal-lymphatic route, Eide et al. (2023) is an intrathecal gadobutrol retention / CSF-to-blood clearance-capacity route in neurological patients, Hirschler et al. (2025) is a region-specific CSF-mobility MRI route, and Dagum et al. (2026) is a model-based overnight biomarker-efflux route under a randomized crossover sleep manipulation. Those rows do not share the same direct observable, carrier class, crossed boundary, time window, intervention regime, or model burden. Therefore, saying only glymphatic route or clearance MRI is still too coarse at the FAQ front door.

At Mind-Upload, the safe reading is now three-axis: name which proxy class and quantity type the route constrains, separately name how specialized, small-cohort, regime-locked, or model-heavy the route still is, and then state what bounded calibrator role the route safely plays. If you skip that third step, you can silently turn "real human route" into "broad hidden-state calibration". If you skip the second, you can silently turn "human evidence got richer" into "human state-complete measurement is close". If you skip the first, you can silently turn "human MRI, PET, or paired-fluid proteomics exists" into "one common latent state is already being measured". The current primary literature does not support any of those jumps.

2026-03-30 addendum: flagship human routes still live on different cohorts and operating points

The next weakness on this page was that even after separating quantity type, a reader could still silently average together papers that were run in different age bands, voxel scopes, stimulation regimes, pathology mixes, and modeling burdens. The primary literature does not support that shortcut. Several current flagship routes are still bounded by cohort composition or method-development scope in the paper itself, so they cannot yet be used as one interchangeable calibration ladder.

Route Verified operating point from the primary paper How this site now reads it
Five-metabolite 1H-MRSI similarity scaffold
Lucchetti et al. (2025)
Main cohort: 51 healthy adolescents aged 13-15 years; replication cohort: 13 healthy controls aged 15-35 years at a different site. A replicated biochemical-similarity scaffold, not a route-free adult human baseline for hidden-state closure.
High-resolution 1H-MRSI metabolite-distribution mapping
Guo et al. (2025)
Ultrahigh-field high-resolution metabolite mapping under extended spatiospectral encoding, subspace modeling, and explicit ghosting / aliasing / low-SNR handling. A specialized metabolite-distribution route, not a route-free baseline, not a similarity scaffold, and not a kinetic-rate map.
Localized functional 31P NAD-dynamics
Kaiser et al. (2026)
25 healthy volunteers; one visual-cortex voxel functionally localized by prior fMRI during a flashing-checkerboard task. A task- and voxel-bounded NAD+ dynamics route, not a whole-brain or task-general energetic-state readout.
Deuterium absolute quantification
Karkouri et al. (2026)
12 healthy volunteers plus 5 treatment-naive glioblastoma patients; only two healthy volunteers were scanned post-glucose in the abstracted protocol. A mixed-cohort quantification-method paper, not a ready-made healthy-human reference atlas or a generic route-free baseline.
Tracer-specific BBB transport PET
Chung et al. (2025)
Five experiments across tracer-comparison and exploratory age / MASLD / blood-glucose applications; the paper states no human ground truth yet and calls for test-retest plus gold-standard CBF validation. A promising molecular BBB-transport method, not yet a settled permeability meter or a direct local controller readout.
Blood-CSF barrier / choroid-plexus perfusion / transport family
Zhao et al. (2020); Sun et al. (2024); Petitclerc et al. (2021, 2026); Anderson et al. (2022); Wu et al. (2026)
A mixed route family: 7 healthy volunteers for early choroid-plexus perfusion, 12 healthy subjects for ultra-long-TE blood-to-CSF transport, 11 cognitively impaired + 28 cognitively normal older adults for DCE water cycling, 6 healthy volunteers for REXI apparent exchange, and a separate 641-person HCP-Aging perfusion analysis for the perfusion lane. A bounded BCSFB / choroid-plexus route family, not a route-free BBB scalar, not a generic clearance baseline, and not a direct epithelial-controller readout.
Paired CSF-plasma protein-balance proteomics
Farinas et al. (2025)
2,171 paired-fluid participants across multiple cohorts, including 931 healthy controls and 1,240 participants with neurodegenerative disease or cognitive impairment; 2,304 proteins were retained for individualized CSF/plasma ratio analysis. A large-cohort paired-fluid barrier-system-balance route, not a route-free BBB or BCSFB permeability scalar, not absolute concentration truth, and not a transporter-identity map.
CSF-mobility MRI
Hirschler et al. (2025)
20 analyzed healthy younger participants at rest, plus a separate 8 CAA / 8 control cohort; the paper also includes a distinct vasomotion-manipulation substudy within the healthy sample. A CSF-mobility map with region-specific physiological drivers, not one universal human clearance baseline or a direct glymphatic-flux meter.
Sleep-linked clearance model
Dagum et al. (2026)
Multi-site randomized crossover; healthy older-adult cohorts from two sites, with 39 participants in the primary trial analysis, measured with an investigational device and a multicompartment model. A sleep-dependent biomarker-efflux route under a named physiological manipulation, not a route-free glymphatic meter or segment-resolved maintenance-controller readout.

What follows directly is that route maturity is not just sample size. It also includes whether the paper is an atlas, a single-voxel task study, a mixed pathology/healthy method paper, an exploratory clinical application, or a sleep-manipulation model study. On this site, those operating-point differences are logged before human rows are composed.

Route name alone is too coarse

On this site, saying only MRI, PET, or even human proxy route is no longer enough. The FAQ now asks one more question before the claim ceiling rises: is the paper reporting similarity, high-resolution 1H-MRSI metabolite distribution, 31P metabolite / pH balance, 31P MT exchange-flux, 31P NAD-content mapping, localized functional 31P NAD dynamics, deuterium absolute metabolite mapping / quantification, deuterium kinetic-rate imaging, tract-scale transmission-speed estimation, bilayer-sensitive myelin contrast, BBB water exchange, tracer-specific BBB transport, paired CSF-plasma protein balance, SMBT-1 MAO-B target validation, SMBT-1 AD-spectrum disease context, SMBT-1 brain quantification, whole-body SMBT-1 biodistribution, SL25.1188 MAO-B disease / severity route, I2BS PET, TSPO disease-context / validation-bounded PET, CSF1R target-defined PET, COX-2 enzyme-defined PET, macroscopic CSF oscillation, parenchyma-CSF water exchange, intrathecal tracer / CSF-to-blood clearance, CSF mobility, or biomarker efflux? If that label is missing, the route stays too coarse to support same-subject state-complete language.

Deuterium route names also need an operating-point split

Karkouri et al. (2026) strengthen a named absolute-quantification route, but the primary paper itself is a mixed healthy / glioblastoma quantification study with only two post-glucose healthy volunteers; Li et al. (2025) strengthen a blood-input kinetic-rate route; Ahmadian et al. (2025) show that dose changes the visibility of downstream deuterated metabolites; and Bøgh et al. (2024) show that repeatability depends on a stated 3 T protocol and time-point window. Therefore, saying only deuterium imaging is still too coarse even after it has been separated from 31P.

A further tightening follows on this site: even if those three axes are logged, the bundle is still not promoted unless the composition audit says whether it passes a robustness gate, a common-driver / quantity-bridge gate, and an increment-over-the-strongest-single-row gate.

Eight quick checks behind the three-gate rule
  • Same route once repeated? Bøgh et al. (2024) showed route-specific repeatability for 3 T DMI under a stated oral-glucose protocol and time-point window, Finnema et al. (2018) showed route-specific mean absolute test-retest reproducibility of 3-9% for regional SV2A PET VT, Holiga et al. (2018) found MRI reliability ranging from poor to excellent across common task-fMRI and resting-fMRI measures, and Wirsich et al. (2021) showed that some simultaneous EEG-fMRI connectome relationships can reproduce across 72 subjects from four centres spanning 1.5T to 7T. So route-local repeatability and cross-site portability have to stay separate.
  • Same quantity? Johansen et al. (2024), Lucchetti et al. (2025), Guo et al. (2025), Ren et al. (2015), Ren et al. (2017), Guo et al. (2024), Kaiser et al. (2026), Karkouri et al. (2026), Li et al. (2025), Morgan et al. (2024), Chung et al. (2025), Farinas et al. (2025), Zhao et al. (2020), Petitclerc et al. (2021), Anderson et al. (2022), Wu et al. (2026), and Dagum et al. (2026) do not report one common object; they report density, similarity, high-resolution metabolite distributions, energetic balance, exchange flux, static NAD content, task-locked local NAD dynamics, deuterium absolute metabolite mapping / quantification, kinetic-rate maps, BBB water exchange, tracer-specific BBB transport, paired-fluid protein balance, choroid-plexus perfusion, blood-to-CSF transport, water cycling, apparent BCSFB exchange, and support-state / efflux proxies.
  • Same driver? Chen et al. (2025) found tightly coupled global progression plus distinct network patterns in simultaneous EEG-PET-MRI, and Bolt et al. (2025) showed that a major global fMRI mode is substantially coupled to autonomic physiology.
  • Same sign? Epp et al. (2025) showed that significant task BOLD changes can coexist with opposite oxygen-metabolism changes across many cortical voxels, so even same-session rows are not automatically one solved state variable.
  • Same cohort / regime? Lucchetti et al. (2025) derive metabolic similarity mainly from adolescents aged 13-15 years with a 15-35-year replication cohort; Hirschler et al. (2025) map CSF mobility in healthy younger adults and a separate CAA cohort; Dagum et al. (2026) test healthy older adults under sleep deprivation; Karkouri et al. (2026) mix 12 healthy volunteers with five treatment-naive glioblastoma patients and only two post-glucose healthy scans; Chung et al. (2025) explicitly frame their age / MASLD / blood-glucose applications as exploratory rather than one matched biological baseline; Villemagne et al. (2022) image a pathology-context MAO-B-linked astrocyte route across the Alzheimer disease continuum; Mesfin et al. (2026) report a six-subject healthy-human whole-body SMBT-1 biodistribution route; and Livingston et al. (2022) show that a human I2BS route varies by region and impairment stage. Cross-row agreement is therefore not one matched human baseline by default.
  • Same bundle once one row drops out or the site changes? Amiri et al. (2023) showed that full EEG+fMRI availability can shrink to a restricted complete-feature subset, while Manasova et al. (2026) showed that multimodal models validated across centres can still display higher inter-modality disagreement in clinically important groups. So a bundle must also survive missing-row and transfer checks.
  • Same conclusion after shared-driver audit? Vafaii et al. (2024) found both common and divergent cross-modal structure, so agreement across rows still has to be separated from modality-specific residuals.
  • Better than the strongest single row? Manasova et al. (2026) is informative precisely because it reports both gains from adding modalities and remaining disagreement. If the paper does not show what the bundle adds over the best individual row under matched conditions, row diversity stays descriptive rather than state-closing.

The same stop line matters even before multimodal fusion. If a bundle crosses developmental stage, aging regime, or pathology enrichment, this site asks for an explicit transfer argument rather than silently importing one cohort's baseline into another.

One more correction is needed before overreading the same literature: the strongest maintenance-state causal papers and the strongest current human-observability papers are often on different ladders. Hadzibegovic et al. (2025), Terceros et al. (2026), and Bukalo et al. (2026) strengthen local causal relevance, while Zrenner et al. (2018), Hirschler et al. (2025), and Dagum et al. (2026) strengthen human perturbation or proxy routes. That combination still does not mean that the responsible human controller was measured. The short crosswalk is in WBE 101: causal relevance vs human observability.

Route What it directly gives you Why it still stops short
Rodent astrocyte causal studies
Cahill et al. (2024); Williamson et al. (2025); Dewa et al. (2025); Bukalo et al. (2026)
Local perturbation-linked evidence that astrocytes can matter for encoding, recall, stabilization, or fear-state support. Not a living-human readout, not a whole-brain route, and not the same spatial unit as human proxy studies.
SMBT-1 MAO-B target-validation / AD-context / quantification routes
Villemagne et al. (2022); Hiraoka et al. (2025)
Brain-side MAO-B PET routes that separately support target validation, AD-context contrast, and named quantification choices. They are still not one generic astrocyte-state meter, one route-free brain baseline, or a content-specific astrocyte-ensemble readout.
SL25.1188 MAO-B disease / severity routes
Matsuoka et al. (2026); Best et al. (2026)
A second MAO-B tracer family whose AD or AUD reading depends on simplified-versus-kinetic quantification and on cohort covariates such as severity and smoking. It is still not an SMBT-1-equivalent family, not an I2BS route, not a route-free astrocyte scalar, and not a local controller readout.
I2BS brain astrocyte PET route
Tyacke et al. (2018); Livingston et al. (2022)
A different target class whose disease-context reading varies with region and impairment stage. It is still not an MAO-B-equivalent family, not a route-free astrocyte scalar, and not a local controller readout.
Whole-body SMBT-1 biodistribution
Mesfin et al. (2026)
Tracer-family biodistribution, excretion, and organ-uptake profile for SMBT-1 in healthy humans. It still does not tell you regional brain astrogliosis burden, AD-context effect size, or which astrocyte controller caused any later disease signal.
Human clearance-transport routes
Fultz et al. (2019); Kim, Huang, & Liu (2025); Lim et al. (2025); Yoo et al. (2025); Eide et al. (2023); Hirschler et al. (2025); Dagum et al. (2026)
Distinct human rows for macroscopic CSF oscillation, parenchyma-CSF water exchange, respiration-conditioned net flow, exercise-conditioned contrast influx / meningeal-lymphatic flow, intrathecal tracer / CSF-to-blood clearance, CSF mobility, and model-based overnight biomarker efflux. Those rows still do not identify which astrocyte, meningeal-lymphatic segment, microglial controller, or synapse caused the effect.
Human target-defined neuroimmune PET routes
Biechele et al. (2023); Wijesinghe et al. (2025); Horti et al. (2022); Ogata et al. (2025); Yan et al. (2025)
Distinct human rows for TSPO disease-context / validation-bounded PET, CSF1R route-setting PET, and COX-2 enzyme-defined PET. Those rows still do not identify which microglial controller, immune-effector program, or local synapse caused the effect, and they do not collapse into one universal human microglia scalar.

A second safety rule follows from the same literature: local human ultrastructure is not simply the first rung of a living-human proxy ladder. On this site it is paired with the Destructive-Structure Route Card because preservation route, live-to-fix window, registration scope, and proofreading burden still change what the paper means.

That caution applies especially to human clearance and neuroimmune papers. On this site, macroscopic CSF oscillation, parenchyma-CSF water exchange, respiration-conditioned net flow, exercise-conditioned contrast influx / meningeal-lymphatic flow, intrathecal tracer / CSF-to-blood clearance, CSF-mobility MRI, and sleep-linked biomarker-efflux studies lower a support-state uncertainty, while TSPO, CSF1R, and COX-2 PET lower a target-defined neuroimmune uncertainty. But none of those rows tells you which meningeal-lymphatic segment, which microglial controller, or which local synapse is responsible for the difference. They therefore stay below a local maintenance-controller claim ceiling.

The shortest follow-up is WBE 101: human observability ladder, Wiki: Human Proxy Composition and Route Maturity, and Wiki: Observability and Claim Ceiling by Measurement Stack. Those pages keep proxy class, route maturity, composition failure modes, and the still-latent hidden-state families in one place. If the argument then promotes same-subject or same-brain wording into one state sample across stages or days, continue directly to Q2e.

Q. If a paper says same-subject or same-brain, does that mean one state was captured?

A. Not automatically. On this site, same-subject or same-brain solves specimen identity, not state continuity. A sequential bridge still has to justify what object / witness is supposed to survive, how failure would have been detected, elapsed time, physiological-regime continuity, coordinate transfer, and bridge validation before one later stage is read as the same state rather than the same specimen at another stage.

The primary literature is already strong enough to require that separation. Lu et al. (2023) showed that preservation route changes extracellular-space retention and native geometry, and Idziak et al. (2023) showed subtle spine-morphology changes plus substantial membrane damage after chemical fixation. Bosch et al. (2022) and MICrONS Consortium et al. (2025) then showed why even very strong correlative same-brain workflows remain multistage local bridges with landmarks, targeted subvolumes, and later reconstruction rather than simultaneous whole-state capture. In other words, the bridge may carry a local correspondence object without carrying one global latent state.

The same warning applies even without fixation. Gallego et al. (2020) showed that a latent manifold can remain stable despite turnover in recorded neurons, Noda et al. (2025) showed recovery of a population-level representational map after selective neuron loss, and Van De Ville et al. (2021) plus Di et al. (2021) showed that fingerprint-like identifiability depends on timescale and feature family. Those are different carried objects, not interchangeable proof that the same full state survived.

Stable performance is also not the same thing as raw continuity. Karpowicz et al. (2025) stabilized decoding by aligning recordings to a consistent latent-dynamics object, Wilson et al. (2025) maintained long-term cursor control through repeated unsupervised recalibration, and Wairagkar et al. (2025) reported a clinically important speech neuroprosthesis while still relying on a bounded fixed-decoder horizon. Benisty et al. (2024) and Egger et al. (2024) further showed that spontaneous behavior and 10-hour EEG dynamics can move the measured state within hours. Therefore, a cross-day or cross-regime bridge still cannot be read as one stable state sample by wording or score alone.

Six checks before raising the claim ceiling

  • Carried object / witness: was the bridge about landmarks, a targeted subvolume, a latent manifold, representational geometry, a fingerprint feature family, or something else?
  • Tolerance / failure rule: what mismatch would have counted as bridge failure, and where was the threshold written?
  • Time window: how much time elapsed, and which state families could drift during that window?
  • Regime continuity: were task, arousal, sleep pressure, anesthesia, pharmacology, or recovery status matched?
  • Coordinate continuity: were landmarks, deformation model, and residual mismatch disclosed?
  • Validation and rescue route: was the bridge itself independently checked, and did the reported score survive without alignment, recalibration, or other rescue steps?

At Mind-Upload, if those fields are missing, we read the result as specimen linkage only, witness-specific continuity only, or at most a sequential local scaffold, not as same-state evidence. The shortest follow-up is Verification: State-Continuity Bridge Card and Wiki: State-Continuity Bridge. If the bridge crosses hours to days in a live stack, add Verification: Temporal Validity Card as well.

Q. Then what should we build to count as progress?

A. For now, L0-L2 is the realistic target: reproducible analyses, comparable benchmarks, and models that can be tested through intervention prediction. Mind-Upload turns those into operating templates, logs, and rules that the site can actually use.

Concrete deliverables

  • Input: BIDS or EEG-BIDS, metadata, and QC logs
  • Procedure: a fixed pipeline, execution logs, and documented failure cases
  • Output: metrics, baseline deltas, and the result of falsification conditions

If you want to see how those three parts connect in a single EEG example, the shortest route is Wiki: Verification example walkthrough.

Q. Why is standardization so important?

A. Without standards, people appear to be talking about the same thing while actually comparing different inputs, different procedures, and different metrics. Once that happens, progress becomes unreadable.

Examples such as the PDB and the BIDS + OpenNeuro ecosystem differ in field, but they share the same crucial property: they turned progress into something different groups could measure in comparable ways. The casework collection summarizes the design pattern, and if you want the role differences among BIDS, OpenNeuro, validators, and benchmarks first, the shortest path is Wiki: Standards, repositories, validators, and benchmarks.

Q. What is the “benchmark trap”?

A. It is the phenomenon where winning on a metric drifts away from the real goal, a version of Goodhart's law. For example, the score may go up because of data leakage or overfitting, or the system may be too costly to deploy in practice. Mind-Upload treats failure cases, leakage checks, and model cards as part of the benchmark design itself.

Wiki: Dataset splits and data leakage collects typical ways the numbers break when train/test separation is poorly designed.

Q. If offline accuracy is high, is that enough for closed loop?

A. No. In a closed loop, the output changes the next input and often the environment as well, so end-to-end latency, jitter, drift, and safe-stop behavior all matter. A method can work well on recorded data and still fail to operate stably in real time.

Recent speech neuroprosthesis work made major progress in real-time text, audio, and voice output. Littlejohn et al. (2025) showed streaming brain-to-voice output every 80 ms, and Wairagkar et al. (2025) showed neural-to-voice synthesis under 10 ms. But those are within-session achievements in invasive communication subsystems, not general evidence for WBE. As Wilson et al. (2025) shows, whether such systems can be maintained long-term while reducing daily supervised recalibration is a separate question.

At Mind-Upload, offline accuracy and L3 closed-loop stability are read separately. In particular, if the work does not report P50/P95/P99 latency, silence or abstention behavior, recalibration burden, and cross-day degradation apart from accuracy, we do not read it as a deployable closed loop. For a beginner-friendly version of that distinction, see Wiki: Closed loop, latency, jitter, and safe stops.

The same front-door caution now applies to adaptive DBS and other burst- or state-triggered neuromodulation. Recent primary literature does not support reading them as one generic `adaptive` success. Beta-guided bradykinesia control, gamma-linked dyskinesia or prokinetic routes, and decoder-based movement-responsive control are different controller families, and movement state, medication state, sensing compatibility, comparator policy, and programming burden can all change what the result means. So on this site, a positive symptom result is not read as generic proof that state-dependent control has been solved unless those controller details are visible.

Q. If latency is low, does that mean the body/environment problem is solved?

A. No. Low latency only tells you that one loop is fast enough; it does not tell you that the relevant subject boundary has been reproduced. Musall et al. (2019) and Stringer et al. (2019) showed that ongoing behavior shapes a large fraction of cortical activity, Saleem et al. (2013) and Ravassard et al. (2013) showed that locomotion, optic flow, vestibular, and other sensory cues reshape cortical and hippocampal codes, Zelano et al. (2016) showed that nasal respiration entrains human limbic activity and modulates memory, and Flesher et al. (2021) showed that adding tactile feedback improves a local bidirectional BCI loop.

That fast-loop disclosure is still not enough by itself. de Quervain et al. (1998) and Oei et al. (2007) showed that glucocorticoid state can impair retrieval and reduce hippocampal / prefrontal retrieval activity, while McCauley et al. (2020), Barone et al. (2023), and Birnie et al. (2023) showed that circadian timing and corticosteroid rhythm alter hippocampal plasticity. At Mind-Upload, a closed-loop paper that does not disclose which sensory, motor, interoceptive, and slow internal-milieu routes were preserved, substituted, matched, perturbed, or omitted, plus what happened when those loops were removed or altered, stays a local controller or local subsystem-loop result. The shortest follow-up is Verification: Body / Environment Boundary Card together with Wiki: before milliseconds, fix which loop boundary was actually preserved, Roadmap M4, and Roadmap I6.

Q. What is the site's stance on the hard problem of consciousness?

A. Mind-Upload does not assume any specific philosophical stance on the hard problem of consciousness (Chalmers, 1995). It uses a functionalist approach as an implementation basis, but it does not claim that functional equivalence is sufficient for phenomenal consciousness. Instead, it evaluates verifiable operational indicators such as PCI-ST, counterfactual tests, and agreement under intervention, and leaves philosophical consequences to the interpretation stage once there is enough empirical data.

Transparency

This is a serious limitation. Even if functional equivalence is confirmed, the identity of phenomenal consciousness is not guaranteed. The site states that limit explicitly and then accumulates only the progress that can still be measured.

Q. How do you handle the copy problem?

A. In a scan-and-copy route, the original and the copy branch immediately after the copy is made, so there is no principled way to decide which one is “the person” in the strong sense associated with identity debates. Mind-Upload therefore centers slow continuous mind uploading as a design strategy, treating continuity of process without abrupt rupture as an engineering requirement.

Even then, the strategy still needs a pre-fixed criterion for when the transfer is complete. Mind-Upload treats that as part of the L4 claim ladder rather than as something already solved.

Q. What happened with experimental tests of IIT and GNWT?

A. The 2025 Cogitate Consortium adversarial collaboration tested predictions from IIT and GNWT at large scale. The result was that neither theory received full support: IIT's posterior cortical sustained activity received only partial support, while GNWT's prefrontal ignition remained difficult to separate from report-related activity. In response, Mind-Upload avoids overcommitting to any one theory and instead emphasizes theory-light empirical indicators such as PCI.

If you want the theory map itself first, Wiki: Consciousness theory map is the shortest route.

Q. How does the site treat ethical issues?

A. WBE brings its own ethical issues, including (1) the legal status and rights of emulated beings, (2) whether consent can be withdrawn, including the right to stop, (3) the ethics of multiple copies, and (4) access inequality and social justice. Mind-Upload places the design of ethical review and governance as a prerequisite for L5 social deployment while focusing current effort on the technical foundation in L0-L2.

Q. How is this different from other WBE-related projects?

A. Relative to several major existing efforts, the rough distinction is:

  • Blue Brain / Human Brain Project: more focused on large-scale simulation. Mind-Upload differs by prioritizing the verification framework first.
  • Whole Brain Architecture Initiative (WBAI): more focused on constructive architecture and roadmap work. Mind-Upload is complementary in that it fixes benchmarks and falsification conditions early.
  • OpenWorm: focused on full-connectome implementation for C. elegans. Mind-Upload instead starts from non-invasive human-brain measurement, especially EEG.

The distinguishing strategy of Mind-Upload is to build the Verification Commons first.

References (FAQ)

  1. Tang, J., et al. (2023). Semantic reconstruction from non-invasive brain recordings. doi:10.1038/s41593-023-01304-9
  2. Défossez, A., Caucheteux, C., Rapin, J., et al. (2023). Decoding speech perception from non-invasive brain recordings. doi:10.1038/s42256-023-00714-5
  3. d'Ascoli, S., Bel, C., Rapin, J., et al. (2025). Towards decoding individual words from non-invasive brain recordings. doi:10.1038/s41467-025-65499-0
  4. Ye, Z., Ai, Q., Liu, Y., de Rijke, M., Zhang, M., Lioma, C., & Ruotsalo, T. (2025). Generative language reconstruction from brain recordings. doi:10.1038/s42003-025-07731-7
  5. Rybár, M., Poli, R., & Daly, I. (2024). Using data from cue presentations results in grossly overestimating semantic BCI performance. doi:10.1038/s41598-024-79309-y
  6. Horikawa, T. (2025). Mind captioning: Evolving descriptive text of mental content from human brain activity. doi:10.1126/sciadv.adw1464
  7. Unnwongse, K., Achakulvisut, T., Wu, J. Y., et al. (2023). Validating EEG source imaging using intracranial electrical stimulation in focal epilepsy. doi:10.1093/braincomms/fcad023
  8. Hao, S., Zhao, H., Feng, Z., et al. (2025). HD-EEG source imaging with simultaneous SEEG recording in drug-resistant epilepsy. doi:10.1111/epi.18552
  9. Mahjoory, K., Nikulin, V. V., Botrel, L., et al. (2017). Consistency of EEG source localization and connectivity estimates. doi:10.1016/j.neuroimage.2017.02.076
  10. Mikulan, E., Russo, S., Parmigiani, S., et al. (2020). Simultaneous human intracerebral stimulation and HD-EEG, ground-truth for source localization methods. doi:10.1038/s41597-020-0467-x
  11. Ahlfors, S. P., Han, J., Belliveau, J. W., & Hämäläinen, M. S. (2010). Sensitivity of MEG and EEG to source orientation. doi:10.1007/s10548-010-0154-x
  12. Ahlfors, S. P., Han, J., Lin, F.-H., Witzel, T., Belliveau, J. W., Hämäläinen, M. S., & Halgren, E. (2010). Cancellation of EEG and MEG signals generated by extended and distributed sources. doi:10.1002/hbm.20851
  13. Goldenholz, D. M., Ahlfors, S. P., Hämäläinen, M. S., Sharon, D., Ishitobi, M., Vaina, L. M., & Stufflebeam, S. M. (2009). Mapping the signal-to-noise-ratios of cortical sources in magnetoencephalography and electroencephalography. doi:10.1002/hbm.20571
  14. Piastra, M. C., Nüßing, A., Vorwerk, J., Clerc, M., Engwer, C., & Wolters, C. H. (2021). A comprehensive study on electroencephalography and magnetoencephalography sensitivity to cortical and subcortical sources. doi:10.1002/hbm.25272
  15. Willett, F. R., Kunz, E. M., Fan, C., et al. (2023). A high-performance speech neuroprosthesis. doi:10.1038/s41586-023-06377-x
  16. Littlejohn, K. T., Dabagia, M., Ladwig, A., et al. (2025). A streaming brain-to-voice neuroprosthesis to restore naturalistic communication. doi:10.1038/s41593-025-01905-6
  17. Wairagkar, M., Card, N. S., Singer-Clark, T., et al. (2025). An instantaneous voice-synthesis neuroprosthesis. doi:10.1038/s41586-025-09127-3
  18. Singh, A., Wu, E., Ramsey, N. F., et al. (2025). Transfer learning via distributed brain recordings enables reliable speech decoding. doi:10.1038/s41467-025-63825-0
  19. Karpowicz, B. M., Ali, Y. H., Wimalasena, L. N., et al. (2025). Stabilizing brain-computer interfaces through alignment of latent dynamics. doi:10.1038/s41467-025-59652-y
  20. Wilson, G. H., Stein, E. A., Kamdar, F., et al. (2025). Long-term unsupervised recalibration of cursor-based intracortical brain-computer interfaces using a hidden Markov model. doi:10.1038/s41551-025-01536-z
  21. Penny, W. D., Stephan, K. E., Mechelli, A., & Friston, K. J. (2004). Comparing dynamic causal models. doi:10.1016/j.neuroimage.2004.03.026
  22. Rosa, M. J., Friston, K., & Penny, W. (2012). Post-hoc selection of dynamic causal models. doi:10.1016/j.jneumeth.2012.04.013
  23. Frässle, S., Paulus, F. M., Krach, S., & Jansen, A. (2016). Test-retest reliability of effective connectivity in the face perception network. doi:10.1002/hbm.23061
  24. Frässle, S., Manjaly, Z. M., Do, C. T., Kasper, L., Pruessmann, K. P., & Stephan, K. E. (2021). Whole-brain estimates of directed connectivity for human connectomics. doi:10.1016/j.neuroimage.2020.117491
  25. Wu, H., Hu, X., & Zeng, Y. (2024). A fast dynamic causal modeling regression method for fMRI. doi:10.1016/j.neuroimage.2024.120954
  26. Almgren, H., Van de Steen, F., Razi, A., Friston, K., & Marinazzo, D. (2020). The effect of global signal regression on DCM estimates of noise and effective connectivity from resting state fMRI. doi:10.1016/j.neuroimage.2019.116435
  27. Zhang, S., Jung, K., Langner, R., Florin, E., Eickhoff, S. B., & Popovych, O. V. (2024). Impact of data processing varieties on DCM estimates of effective connectivity from task-fMRI. doi:10.1002/hbm.26751
  28. Ma, L., Braun, S. E., Steinberg, J. L., Bjork, J. M., Martin, C. E., Keen II, L. D., & Moeller, F. G. (2024). Effect of scanning duration and sample size on reliability in resting state fMRI dynamic causal modeling analysis. doi:10.1016/j.neuroimage.2024.120604
  29. Jafarian, A., Assem, M. K., Kocagoncu, E., et al. (2024). Reliability of dynamic causal modelling of resting-state magnetoencephalography. doi:10.1002/hbm.26782
  30. Gouwens, N. W., et al. (2021). Integrated morphoelectric and transcriptomic classification of cortical GABAergic cells. doi:10.1038/s41586-020-2907-3
  31. Hengen, K. B., Torrado Pacheco, A., McGregor, J. N., Van Hooser, S. D., & Turrigiano, G. G. (2016). Neuronal firing rate homeostasis is inhibited by sleep and promoted by wake. doi:10.1016/j.cell.2016.01.046
  32. Torrado Pacheco, A., et al. (2021). Sleep Promotes Downward Firing Rate Homeostasis. doi:10.1016/j.neuron.2021.04.004
  33. Xu, W., et al. (2024). Sleep restores an optimal computational regime in cortical networks. doi:10.1038/s41467-024-47838-5
  34. Ngo, H.-V. V., Martinetz, T., Born, J., & Mölle, M. (2013). Auditory closed-loop stimulation of the sleep slow oscillation enhances memory. doi:10.1016/j.neuron.2013.03.006
  35. Whitmore, N. W., Bassard, A. M., & Paller, K. A. (2022). Targeted memory reactivation of face-name learning depends on ample and undisturbed slow-wave sleep. npj Science of Learning, 7, 1. doi:10.1038/s41539-021-00119-2
  36. Baxter, B. S., Mylonas, D., Kwok, K. S., Talbot, C. E., Patel, R., Zhu, L., Vangel, M., Stickgold, R., & Manoach, D. S. (2023). The effects of closed-loop auditory stimulation on sleep oscillatory dynamics in relation to motor procedural memory consolidation. Sleep, 46(10), zsad206. doi:10.1093/sleep/zsad206
  37. Schreiner, T., Petzka, M., Staudigl, T., & Staresina, B. P. (2021). Endogenous memory reactivation during sleep in humans is clocked by slow oscillation-spindle complexes. doi:10.1038/s41467-021-23520-2
  38. Schreiner, T., Petzka, M., Staudigl, T., et al. (2023). Respiration modulates sleep oscillations and memory reactivation in humans. Nature Communications, 14, 8351. doi:10.1038/s41467-023-43450-5
  39. Geva-Sagiv, M., Mankin, E. A., Eliashiv, D., et al. (2023). Augmenting hippocampal-prefrontal neuronal synchrony during sleep enhances memory consolidation in humans. doi:10.1038/s41593-023-01324-5
  40. Schreiner, T., Griffiths, B. J., Kutlu, M., et al. (2024). Spindle-locked ripples mediate memory reactivation during human NREM sleep. doi:10.1038/s41467-024-49572-8
  41. Whitmore, N. W., Yamazaki, E. M., & Paller, K. A. (2024). Targeted memory reactivation with sleep disruption does not weaken week-old memories. npj Science of Learning, 9, 64. doi:10.1038/s41539-024-00276-0
  42. Jourde, N., Fattinger, S., Teague, M., et al. (2025). The effectiveness of auditory stimulation in sleep varies with thalamocortical spindle phase. doi:10.1016/j.neuroimage.2025.121530
  43. Duan, W., Xu, Z., Chen, D., et al. (2025). Electrophysiological signatures underlying variability in human memory consolidation. doi:10.1038/s41467-025-57766-x
  44. Shin, G.-H., Kweon, Y.-S., Oh, S., et al. (2025). Personalized targeted memory reactivation enhances consolidation of challenging memories via slow wave and spindle dynamics. doi:10.1038/s41539-025-00340-3
  45. Gibson, E. M., et al. (2014). Neuronal activity promotes oligodendrogenesis and adaptive myelination in the mammalian brain. doi:10.1126/science.1252304
  46. McKenzie, I. A., et al. (2014). Motor skill learning requires active central myelination. doi:10.1126/science.1254960
  47. Looser, Z. J., et al. (2024). Oligodendrocyte-axon metabolic coupling is mediated by extracellular K+ and maintains axonal health. doi:10.1038/s41593-023-01558-3
  48. Hardingham, N. R., & Larkman, A. U. (1998). The reliability of excitatory synaptic transmission in slices of rat visual cortex in vitro is temperature dependent. doi:10.1111/j.1469-7793.1998.249bu.x
  49. Volgushev, M., Vidyasagar, T. R., Chistiakova, M., Yousef, T., & Eysel, U. T. (2000). Membrane properties and spike generation in rat visual cortical cells during reversible cooling. doi:10.1111/j.1469-7793.2000.00059.x
  50. Moser, E., Mathiesen, I., & Andersen, P. (1993). Association between brain temperature and dentate field potentials in exploring and swimming rats. doi:10.1126/science.8446900
  51. Long, M. A., & Fee, M. S. (2008). Using temperature to analyse temporal dynamics in the songbird motor pathway. doi:10.1038/nature07448
  52. Rangaraju, V., Calloway, N., & Ryan, T. A. (2014). Activity-driven local ATP synthesis is required for synaptic function. doi:10.1016/j.cell.2013.12.042
  53. Rangaraju, V., Lauterbach, M., & Schuman, E. M. (2019). Spatially stable mitochondrial compartments fuel local translation during plasticity. doi:10.1016/j.cell.2018.12.013
  54. Divakaruni, S. S., Van Dyke, A. M., Chandra, R., et al. (2018). Long-term potentiation requires a rapid burst of dendritic mitochondrial fission during induction. doi:10.1016/j.neuron.2018.09.025
  55. Bapat, P., Nirschl, J. J., Wilkerson, J. R., et al. (2024). VAP stabilizes dendritic mitochondria to locally support synaptic plasticity. doi:10.1038/s41467-023-44233-8
  56. Hu, H., Tang, J., Wu, Y., et al. (2025). Polarized ATP synthase in synaptic mitochondria induced by learning and plasticity signals. doi:10.1038/s42003-025-08963-3
  57. Park, M., Salgado, J. M., Ostroff, L., Helton, T. D., Robinson, C. G., Harris, K. M., & Ehlers, M. D. (2006). Plasticity-induced growth of dendritic spines by exocytic trafficking from recycling endosomes. doi:10.1016/j.neuron.2006.09.040
  58. Zhao, J., Fok, A. H. K., Fan, R., Kwan, P.-Y., Chan, H.-L., Lo, L. H.-Y., Chan, Y.-S., Yung, W.-H., Huang, J., Lai, C. S. W., & Lai, K.-O. (2020). Specific depletion of the motor protein KIF5B leads to deficits in dendritic transport, synaptic plasticity and memory. doi:10.7554/eLife.53456
  59. Swarnkar, S., Avchalumov, Y., Espadas, I., Grinman, E., Liu, X.-A., Raveendra, B. L., Zucca, A., Mediouni, S., Sadhu, A., Valente, S., Page, D., Miller, K., & Puthanveettil, S. V. (2021). Molecular motor protein KIF5C mediates structural plasticity and long-term memory by constraining local translation. doi:10.1016/j.celrep.2021.109369
  60. Rzechorzek, N. M., Thrippleton, M. J., Chappell, F. M., et al. (2022). A daily temperature rhythm in the human brain predicts survival after brain injury. doi:10.1093/brain/awab466
  61. Ren, J., Sherry, A. D., & Malloy, C. R. (2015). 31P-MRS of healthy human brain: ATP synthesis, metabolite concentrations, pH, and T1 relaxation times. doi:10.1002/nbm.3384
  62. Ren, J., Sherry, A. D., & Malloy, C. R. (2017). Efficient 31P band inversion transfer approach for measuring creatine kinase activity, ATP synthesis, and molecular dynamics in the human brain at 7 T. doi:10.1002/mrm.26560
  63. Guo, R., Yang, S., Wiesner, H. M., et al. (2024). Mapping intracellular NAD content in entire human brain using phosphorus-31 MR spectroscopic imaging at 7 Tesla. doi:10.3389/fnins.2024.1389111
  64. Kaiser, A., Vind, F. A., Duarte, J. M. N., et al. (2026). Ultra-high field 31P functional magnetic resonance spectroscopy reveals NAD+ dynamics in brain energy metabolism during visual stimulation. doi:10.1177/0271678X261415784
  65. Karkouri, J., Novoselova, M., Rodgers, C. T., et al. (2026). Absolute Quantification of Brain Deuterium Metabolic Imaging in Healthy Volunteers and Glioblastoma Patients at 7T. doi:10.1002/mrm.70308
  66. Li, X., Zhu, X.-H., Li, Y., et al. (2025). Quantitative mapping of key glucose metabolic rates in the human brain using dynamic deuterium magnetic resonance spectroscopic imaging. doi:10.1093/pnasnexus/pgaf072
  67. Guo, R., Li, Y., Zhao, Y., et al. (2025). High-Resolution Brain Metabolic Imaging at Ultrahigh Field Using Extended Spatiospectral Encoding and Subspace Modeling. doi:10.1109/TBME.2025.3572448
  68. Ahmadian, N., Karkouri, J., Deelchand, D. K., et al. (2025). Human Brain Deuterium Metabolic Imaging at 7 T: Impact of Different [6,6'-2H2]Glucose Doses. doi:10.1002/jmri.29532
  69. Bøgh, N., Vaeggemose, M., Schulte, R. F., et al. (2024). Repeatability of deuterium metabolic imaging of healthy volunteers at 3 T. doi:10.1186/s41747-024-00426-4
  70. Giese, K. P., Fedorov, N. B., Filipkowski, R. K., & Silva, A. J. (1998). Autophosphorylation at Thr286 of the alpha calcium-calmodulin kinase II in LTP and learning. doi:10.1126/science.279.5352.870
  71. Lee, H.-K., Barbarosie, M., Kameyama, K., Bear, M. F., & Huganir, R. L. (2003). Regulation of distinct AMPA receptor phosphorylation sites during bidirectional synaptic plasticity. doi:10.1016/S0092-8674(03)00122-3
  72. Rodrigues, S. M., Farb, C. R., Bauer, E. P., LeDoux, J. E., & Schafe, G. E. (2004). Pavlovian fear conditioning regulates Thr286 autophosphorylation of Ca2+/calmodulin-dependent protein kinase II at lateral amygdala synapses. doi:10.1523/JNEUROSCI.5303-03.2004
  73. Tomita, S., Stein, V., Stocker, T. J., Nicoll, R. A., & Bredt, D. S. (2005). Bidirectional synaptic plasticity regulated by phosphorylation of stargazin-like TARPs. doi:10.1016/j.neuron.2005.01.009
  74. Vierra, N. C., et al. (2023). Endoplasmic reticulum-plasma membrane junctions couple electrical activity to Ca2+-activated PKA signaling in neurons. doi:10.1038/s41467-023-40930-6
  75. Biswas, D., et al. (2023). The landscape of the human brain phosphoproteome reveals region-specific phosphorylation events. doi:10.1021/acs.jproteome.2c00244
  76. Shapson-Coe, A., Januszewski, M., Berger, D. R., et al. (2024). A petavoxel fragment of human cerebral cortex reconstructed at nanoscale resolution. doi:10.1126/science.adk4858
  77. Johansen, A., Beliveau, V., Colliander, E., et al. (2024). An In Vivo High-Resolution Human Brain Atlas of Synaptic Density. doi:10.1523/JNEUROSCI.1750-23.2024
  78. Lucchetti, F., Céléreau, E., Steullet, P., et al. (2025). Constructing the human brain metabolic connectome with MR spectroscopic imaging reveals cerebral biochemical organization. doi:10.1038/s41467-025-66124-w
  79. van Blooijs, D., Nunes, A., van den Boom, M. A., et al. (2023). Developmental trajectory of transmission speed in the human brain. doi:10.1038/s41593-023-01272-0
  80. Morgan, C. A., Thomas, D. L., Shao, X., et al. (2024). Measurement of blood-brain barrier water exchange rate using diffusion-prepared and multi-echo arterial spin labelling: Comparison of quantitative values and age dependence. doi:10.1002/nbm.5256
  81. Baadsvik, E. L., Weiger, M., Froidevaux, R., Schildknecht, C. M., Ineichen, B. V., & Pruessmann, K. P. (2024). Myelin bilayer mapping in the human brain in vivo. doi:10.1002/mrm.29998
  82. Chung, K. J., Abdelhafez, Y. G., Spencer, B. A., et al. (2025). Quantitative PET imaging and modeling of molecular blood-brain barrier permeability. doi:10.1038/s41467-025-58356-7
  83. Farinas, A., Rutledge, J., Bot, V. A., et al. (2025). Disruption of the cerebrospinal fluid-plasma protein balance in cognitive impairment and aging. doi:10.1038/s41591-025-03831-3
  84. Fultz, N. E., Bonmassar, G., Setsompop, K., et al. (2019). Coupled electrophysiological, hemodynamic, and cerebrospinal fluid oscillations in human sleep. doi:10.1126/science.aax5440
  85. Kim, D., Huang, Y., & Liu, J. (2025). Non-invasive MRI measurements of age-dependent in vivo human glymphatic exchange using magnetization transfer spin labeling. doi:10.1016/j.neuroimage.2025.121142
  86. Eide, P. K., Lashkarivand, A., Pripp, A., et al. (2023). Plasma neurodegeneration biomarker concentrations associate with glymphatic and meningeal lymphatic measures in neurological disorders. doi:10.1038/s41467-023-37685-5
  87. Hirschler, L., Runderkamp, B. A. R., Decker, A., et al. (2025). Region-specific drivers of CSF mobility measured with MRI in humans. doi:10.1038/s41593-025-02073-3
  88. Dagum, P., Elbert, D. L., Giovangrandi, L., et al. (2026). The glymphatic system clears amyloid beta and tau from brain to plasma in humans. doi:10.1038/s41467-026-68374-8
  89. Finnema, S. J., Nabulsi, N. B., Mercier, J., et al. (2018). Kinetic evaluation and test-retest reproducibility of [11C]UCB-J, a novel radioligand for positron emission tomography imaging of synaptic vesicle glycoprotein 2A in humans. doi:10.1177/0271678X17724947
  90. Holiga, S., Sambataro, F., Luzy, C., et al. (2018). Test-retest reliability of task-based and resting-state blood oxygen level dependence and cerebral blood flow measures. doi:10.1371/journal.pone.0206583
  91. Wirsich, J., Jorge, J., Iannotti, G. R., et al. (2021). The relationship between EEG and fMRI connectomes is reproducible across simultaneous EEG-fMRI studies from 1.5T to 7T. doi:10.1016/j.neuroimage.2021.117864
  92. Vafaii, H., Mandino, F., Desrosiers-Grégoire, G., et al. (2024). Multimodal measures of spontaneous brain activity reveal both common and divergent patterns of cortical functional organization. doi:10.1038/s41467-023-44363-z
  93. Amiri, M., Fisher, P. M., Raimondo, F., et al. (2023). Multimodal prediction of residual consciousness in the intensive care unit: the CONNECT-ME study. doi:10.1093/brain/awac335
  94. Bolt, T., Wang, S., Nomi, J. S., et al. (2025). Autonomic physiological coupling of the global fMRI signal. doi:10.1038/s41593-025-01945-y
  95. Manasova, V., et al. (2026). Multimodal multicentre investigation of diagnostic and prognostic markers in disorders of consciousness. doi:10.1093/brain/awaf412
  96. Louveau, A., Smirnov, I., Keyes, T. J., et al. (2015). Structural and functional features of central nervous system lymphatic vessels. doi:10.1038/nature14432
  97. Ahn, J. H., Cho, H., Kim, J.-H., et al. (2019). Meningeal lymphatic vessels at the skull base drain cerebrospinal fluid. doi:10.1038/s41586-019-1419-5
  98. Kim, J., et al. (2025). Meningeal lymphatics-microglia axis regulates synaptic physiology. doi:10.1016/j.cell.2025.02.022
  99. Eide, P. K., & Ringstad, G. (2021). Sleep deprivation impairs molecular clearance from the human brain. doi:10.1093/brain/awaa443
  100. Qian, Y., Zhao, T., Zheng, H., Weimer, J., & Boada, F. E. (2012). High-resolution sodium imaging of human brain at 7 T. doi:10.1002/mrm.23225
  101. Qian, Y., Lin, Y.-C., Chen, X., et al. (2025). Single-quantum sodium MRI at 3 T for separation of mono- and bi-T2 sodium signals. doi:10.1038/s41598-025-07800-1
  102. Galarreta, M., & Hestrin, S. (1999). A network of fast-spiking cells in the neocortex connected by electrical synapses. doi:10.1038/47029
  103. Anastassiou, C. A., Perin, R., Markram, H., & Koch, C. (2011). Ephaptic coupling of cortical neurons. doi:10.1038/nn.2727
  104. Graydon, C. W., Cho, S., Diamond, J. S., Kachar, B., von Gersdorff, H., & Grimes, W. N. (2014). Specialized postsynaptic morphology enhances neurotransmitter dilution and high-frequency signaling at an auditory synapse. doi:10.1523/JNEUROSCI.4493-13.2014
  105. Kilb, W., Dierkes, P. W., Syková, E., Vargová, L., & Luhmann, H. J. (2006). Hypoosmolar conditions reduce extracellular volume fraction and enhance epileptiform activity in the CA3 region of the immature rat hippocampus. doi:10.1002/jnr.20871
  106. Xie, L., Kang, H., Xu, Q., Chen, M. J., Liao, Y., Thiyagarajan, M., O'Donnell, J., Christensen, D. J., Nicholson, C., Iliff, J. J., Takano, T., Deane, R., & Nedergaard, M. (2013). Sleep drives metabolite clearance from the adult brain. doi:10.1126/science.1241224
  107. Lauderdale, K., Murphy, T., Tung, T., Davila, D., Binder, D. K., & Fiacco, T. A. (2015). Osmotic Edema Rapidly Increases Neuronal Excitability Through Activation of NMDA Receptor-Dependent Slow Inward Currents in Juvenile and Adult Hippocampus. doi:10.1177/1759091415605115
  108. Burman, R. J., Brodersen, P. J. N., Raimondo, J. V., Sen, A., & Akerman, C. J. (2023). Active cortical networks promote shunting fast synaptic inhibition in vivo. doi:10.1016/j.neuron.2023.08.005
  109. Yang, Y.-C., Wang, G.-H., Chou, P., Hsueh, S.-W., Lai, Y.-C., & Kuo, C.-C. (2024). Dynamic electrical synapses rewire brain networks for persistent oscillations and epileptogenesis. doi:10.1073/pnas.2313042121
  110. Selfe, J. S., et al. (2024). All-optical reporting of inhibitory receptor driving force in the nervous system. doi:10.1038/s41467-024-53074-y
  111. Voldsbekk, I., Maximov, I. I., Zak, N., Roelfs, D., Geier, O., Due-Tønnessen, P., Elvsåshagen, T., Strømstad, M., Bjørnerud, A., & Groote, I. (2020). Evidence for wakefulness-related changes to extracellular space in human brain white matter from diffusion-weighted MRI. doi:10.1016/j.neuroimage.2020.116682
  112. Feld, G. B., Niethard, N., Liu, J., et al. (2026). Electrical Synapses Contribute to Sleep-Dependent Declarative Memory Retention. doi:10.1111/ejn.70401
  113. Suzuki, A., et al. (2011). Astrocyte-neuron lactate transport is required for long-term memory formation. doi:10.1016/j.cell.2011.02.018
  114. Silva, B., et al. (2022). Glial ketogenesis regulates memory maintenance during starvation. doi:10.1038/s42255-022-00528-6
  115. Pavlowsky, A., et al. (2025). Neuronal fatty acid oxidation fuels memory after intensive learning in Drosophila. doi:10.1038/s42255-025-01416-5
  116. Greda, A. K., et al. (2025). Interaction of sortilin with apolipoprotein E3 enables neurons to use long-chain fatty acids as alternative metabolic fuel. doi:10.1038/s42255-025-01389-5
  117. Cahill, M. K., et al. (2024). Network-level encoding of local neurotransmitters in cortical astrocytes. doi:10.1038/s41586-024-07311-5
  118. Williamson, N. R., et al. (2025). Learning-associated astrocyte ensembles regulate memory recall. doi:10.1038/s41586-024-08170-w
  119. Dewa, K., et al. (2025). The astrocytic ensemble acts as a multiday trace to stabilize memory. doi:10.1038/s41586-025-09619-2
  120. Villemagne, V. L., Harada, R., Dore, V., et al. (2022). First-in-Humans Evaluation of 18F-SMBT-1, a Novel 18F-Labeled Monoamine Oxidase-B PET Tracer for Imaging Reactive Astrogliosis. doi:10.2967/jnumed.121.263254
  121. Villemagne, V. L., Harada, R., Dore, V., et al. (2022). Assessing Reactive Astrogliosis with 18F-SMBT-1 Across the Alzheimer Disease Spectrum. doi:10.2967/jnumed.121.263255
  122. Hiraoka, K., Mesfin, B., Wu, Y., et al. (2025). Kinetic and quantitative analysis of [18F]SMBT-1 PET imaging for monoamine oxidase B. doi:10.1007/s12149-025-02083-y
  123. Mesfin, B., Ishioka, Y., Ichinose, Y., et al. (2026). Whole-body biodistribution of [18F]SMBT-1: a novel PET tracer for monoamine oxidase B imaging in healthy humans. doi:10.1007/s12149-025-02144-2
  124. Tyacke, R. J., Myers, J. F. M., Venkataraman, A., et al. (2018). Evaluation of 11C-BU99008, a PET Ligand for the Imidazoline2 Binding Site in Human Brain. doi:10.2967/jnumed.118.208009
  125. Livingston, N. R., Calsolaro, V., Hinz, R., et al. (2022). Relationship between astrocyte reactivity, using novel 11C-BU99008 PET, and glucose metabolism, grey matter volume and amyloid load in cognitively impaired individuals. doi:10.1038/s41380-021-01429-y
  126. Best, L. M., Truong, J., McCluskey, T., et al. (2026). MAO-B status in alcohol use disorder: a [11C]SL25.1188 PET imaging study of putative astrogliosis. doi:10.1038/s41380-025-03355-9
  127. Jaisa-Aad, M., Muñoz-Castro, C., Healey, M. A., Hyman, B. T., & Serrano-Pozo, A. (2024). Characterization of monoamine oxidase-B (MAO-B) as a biomarker of reactive astrogliosis in Alzheimer's disease and related dementias. doi:10.1007/s00401-024-02712-2
  128. Bukalo, O., et al. (2026). Astrocytes enable amygdala neural representations supporting memory. doi:10.1038/s41586-025-10068-0
  129. Lee, J.-C., Wang, C.-Y., Lin, C.-L., & Lu, H.-C. (2022). Synaptic memory survives molecular turnover. doi:10.1073/pnas.2211572119
  130. Musall, S., Kaufman, M. T., Juavinett, A. L., Gluf, S., & Churchland, A. K. (2019). Single-trial neural dynamics are dominated by richly varied movements. doi:10.1038/s41593-019-0502-4
  131. Mostert, P., Albers, A. M., Brinkman, L., Todorova, L., & de Lange, F. P. (2018). Eye Movement-Related Confounds in Neural Decoding of Visual Working Memory Representations. doi:10.1523/ENEURO.0401-17.2018
  132. McFarland, D. J., McCane, L. M., David, S. V., & Wolpaw, J. R. (2005). Brain-computer interface operation: signal and noise during early training sessions. doi:10.1088/1741-2560/2/4/014
  133. Chaibub Neto, E., Pratap, A., Perumal, T. M., et al. (2019). Identity confounding in machine learning can be controlled by design. doi:10.1038/s41746-019-0178-x
  134. Xu, M., Fanton, S., Jahanbekam, A., et al. (2020). The Cross-Dataset Variability Problem in EEG Decoding With Deep Learning. doi:10.3389/fnhum.2020.00103
  135. Jiang, Y., Li, Y., Jia, Y., et al. (2024). Large Brain Model for Learning Generic Representations with Tremendous EEG Data in BCI. ICLR 2024 paper
  136. Lee, N., Barmpas, K., Panagakis, Y., Adamos, D., Laskaris, N., & Zafeiriou, S. (2025). Are Large Brainwave Foundation Models Capable Yet? Insights from Fine-Tuning. PMLR 267
  137. Han, D. D., Lee, A. L., Lee, T., et al. (2025). DIVER-0: A Fully Channel Equivariant EEG Foundation Model. arXiv:2507.14141
  138. Chen, Z., Qin, C., You, W., et al. (2025). HEAR: An EEG Foundation Model with Heterogeneous Electrode Adaptive Representation. arXiv:2510.12515
  139. El Ouahidi, Y., Lys, J., Thölke, P., et al. (2025). REVE: A Foundation Model for EEG -- Adapting to Any Setup with Large-Scale Pretraining on 25,000 Subjects. arXiv:2510.21585
  140. Ma, J., Wu, F., Xing, Y., et al. (2026). Structured Prototype-Guided Adaptation for EEG Foundation Models. arXiv:2602.17251
  141. Liu, D., Chen, Y., Chen, Z., et al. (2026). EEG Foundation Models: Progresses, Benchmarking, and Open Problems. arXiv:2601.17883
  142. Lahiri, J. B., Runwal, P., Kulkarni, A., et al. (2026). PRISM: Exploring Heterogeneous Pretrained EEG Foundation Model Transfer to Clinical Differential Diagnosis. arXiv:2603.02268
  143. EEG Challenge (2025). Official homepage. eeg2025.github.io
  144. EEG Challenge (2025). Rules. Rules page
  145. EEG Challenge (2025). Submission. Submission page
  146. EEG Challenge (2025). Leaderboard. Leaderboard page
  147. Murphy, K., Harris, A. D., & Wise, R. G. (2011). Robustly measuring vascular reactivity differences with breath-hold: normalising stimulus-evoked and resting state BOLD fMRI data. doi:10.1016/j.neuroimage.2010.07.059
  148. Williams, R. J., Specht, J. L., Mazerolle, E. L., et al. (2023). Correspondence between BOLD fMRI task response and cerebrovascular reactivity across the cerebral cortex. doi:10.3389/fphys.2023.1167148
  149. Yücel, M. A., Selb, J., Huppert, T. J., Franceschini, M. A., & Boas, D. A. (2015). Short separation regression improves statistical significance and better localizes the hemodynamic response obtained by near-infrared spectroscopy for tasks with differing autonomic responses. doi:10.1117/1.NPh.2.3.035005
  150. Epp, S. M., Halani, S., Paquette, M., et al. (2025). BOLD signal changes can oppose oxygen metabolism across the human cortex. doi:10.1038/s41593-025-02132-9
  151. Vinck, M., Oostenveld, R., van Wingerden, M., Battaglia, F., & Pennartz, C. M. A. (2011). An improved index of phase-synchronization for electrophysiological data in the presence of volume-conduction, noise and sample-size bias. doi:10.1016/j.neuroimage.2011.01.055
  152. Haufe, S., Nikulin, V. V., Müller, K.-R., & Nolte, G. (2013). A critical assessment of connectivity measures for EEG data: A simulation study. doi:10.1016/j.neuroimage.2012.09.036
  153. Palva, J. M., Wang, S. H., Palva, S., Zhigalov, A., Monto, S., Brookes, M. J., Schoffelen, J.-M., & Jerbi, K. (2018). Ghost interactions in MEG/EEG source space: A note of caution on inter-areal coupling measures. doi:10.1016/j.neuroimage.2018.02.032
  154. Ye, S., Kitajo, K., & Kitano, K. (2020). Information-theoretic approach to detect directional information flow in EEG signals induced by TMS. doi:10.1016/j.neures.2019.09.003
  155. Miljevic, A., Murphy, O. W., Fitzgerald, P. B., & Bailey, N. W. (2025). Estimating sensor-space EEG connectivity PART 1: Identifying best performing methods for functional connectivity in simulated data. doi:10.1016/j.clinph.2025.03.043
  156. Bérut, A., Arakelyan, A., Petrosyan, A., et al. (2012). Experimental verification of Landauer’s principle linking information and thermodynamics. doi:10.1038/nature10872
  157. Attwell, D., & Laughlin, S. B. (2001). An energy budget for signaling in the grey matter of the brain. doi:10.1097/00004647-200110000-00001
  158. Lynn, C. W., Cornblath, E. J., Papadopoulos, L., et al. (2021). Broken detailed balance and entropy production in the human brain. doi:10.1073/pnas.2109889118
  159. Deco, G., Sanz Perl, Y., Bocaccio, H., Tagliazucchi, E., & Kringelbach, M. L. (2022). The INSIDEOUT framework provides precise signatures of the balance of intrinsic and extrinsic dynamics in brain states. doi:10.1038/s42003-022-03505-7
  160. de la Fuente, L. A., Zamberlan, F., Bocaccio, H., et al. (2023). Temporal irreversibility of neural dynamics as a signature of consciousness. doi:10.1093/cercor/bhac177
  161. Nartallo-Kaluarachchi, R., Bonetti, L., Fernández-Rubio, G., et al. (2025). Multilevel irreversibility reveals higher-order organization of nonequilibrium interactions in human brain dynamics. doi:10.1073/pnas.2408791122
  162. Ishihara, K., & Shimazaki, H. (2025). State-space kinetic Ising model reveals task-dependent entropy flow in sparsely active nonequilibrium neuronal dynamics. doi:10.1038/s41467-025-66669-w
  163. Martínez, I. A., Bisker, G., Horowitz, J. M., & Parrondo, J. M. R. (2019). Inferring broken detailed balance in the absence of observable currents. doi:10.1038/s41467-019-11051-w
  164. Blom, K., Song, K., Vouga, E., Godec, A., & Makarov, D. E. (2024). Milestoning estimators of dissipation in systems observed at a coarse resolution. doi:10.1073/pnas.2318333121
  165. Grubb, M. S., & Burrone, J. (2010). Activity-dependent relocation of the axon initial segment fine-tunes neuronal excitability. doi:10.1038/nature09160
  166. Thomas, C., Ye, F. Q., Irfanoglu, M. O., Modi, P., Saleem, K. S., Leopold, D. A., & Pierpaoli, C. (2014). Anatomical accuracy of brain connections derived from diffusion MRI tractography is inherently limited. doi:10.1073/pnas.1405672111
  167. Reveley, C., Seth, A. K., Pierpaoli, C., Silva, A. C., Yu, D., Saunders, R. C., Leopold, D. A., & Ye, F. Q. (2015). Superficial white matter fiber systems impede detection of long-range cortical connections in diffusion MR tractography. doi:10.1073/pnas.1418198112
  168. Donahue, C. J., Sotiropoulos, S. N., Jbabdi, S., Hernandez-Fernandez, M., Behrens, T. E., Dyrby, T. B., Coalson, T., Kennedy, H., Knoblauch, K., Van Essen, D. C., & Glasser, M. F. (2016). Using diffusion tractography to predict cortical connection strength and distance: A quantitative comparison with tracers in the monkey. doi:10.1523/JNEUROSCI.0493-16.2016
  169. Schilling, K. G., Petit, L., Rheault, F., Remedios, S., Pierpaoli, C., Anderson, A. W., Landman, B. A., & Descoteaux, M. (2020). Brain connections derived from diffusion MRI tractography can be highly anatomically accurate if we know where white matter pathways start, where they end, and where they do not go. doi:10.1007/s00429-020-02129-z
  170. Grisot, G., Haber, S. N., Hawrylycz, M., Yendiki, A., et al. (2021). Diffusion MRI and anatomic tracing in the same brain reveal common failure modes of tractography. doi:10.1016/j.neuroimage.2021.118300
  171. Gajwani, M., Oldham, S., Pang, J. C., Arnatkevičiūtė, A., Tiego, J., Bellgrove, M. A., & Fornito, A. (2023). Can hubs of the human connectome be identified consistently with diffusion MRI? doi:10.1162/netn_a_00324
  172. Sarwar, T., Ramamohanarao, K., Daducci, A., Schiavi, S., Smith, R. E., & Zalesky, A. (2023). Evaluation of tractogram filtering methods using human-like connectome phantoms. doi:10.1016/j.neuroimage.2023.120376
  173. He, Y., Hong, Y., Wu, Y., et al. (2024). Spherical-deconvolution informed filtering of tractograms changes laterality of structural connectome. doi:10.1016/j.neuroimage.2024.120904
  174. McMaster, E. M., Newlin, N. R., Rudravaram, G., et al. (2025). Harmonized connectome resampling for variance in voxel sizes. doi:10.1016/j.mri.2025.110424
  175. Manzano-Patrón, J. P., Deistler, M., Schröder, C., et al. (2025). Uncertainty mapping and probabilistic tractography using Simulation-based Inference in diffusion MRI: A comparison with classical Bayes. doi:10.1016/j.media.2025.103580
  176. Zhu, S., Huszar, I. N., Cottaar, M., et al. (2025). Imaging the structural connectome with hybrid MRI-microscopy tractography. doi:10.1016/j.media.2025.103498
  177. Bramati, I. B., Szczupak, D., Carneiro Monteiro, M., Meireles, F., Menezes Guimarães, D., Dean, R. J., Paul, L. K., & Tovar-Moll, F. (2026). Diffusion MRI sampling schemes bias diffusion metrics and tractography. doi:10.3389/fnimg.2026.1670604
  178. Huber, R., Mäki, H., Rosanova, M., Casarotto, S., Canali, P., Casali, A. G., Tononi, G., & Massimini, M. (2013). Human cortical excitability increases with time awake. doi:10.1093/cercor/bhs014
  179. Kuhn, M., Wolf, E., Maier, J. G., Mainberger, F., Feige, B., Schmid, H., et al. (2016). Sleep recalibrates homeostatic and associative synaptic plasticity in the human cortex. doi:10.1038/ncomms12455
  180. Zrenner, C., Desideri, D., Belardinelli, P., & Ziemann, U. (2018). Real-time EEG-defined excitability states determine efficacy of TMS-induced plasticity in human motor cortex. doi:10.1016/j.brs.2017.11.016
  181. Fehér, K. D., Henckaerts, P., Hirsch, V., Bucsenez, U., Kuhn, M., Maier, J. G., et al. (2026). A nap can recalibrate homeostatic and associative synaptic plasticity in the human cortex. doi:10.1016/j.neuroimage.2026.121723
  182. Santoni, G., et al. (2024). Chromatin plasticity predetermines neuronal eligibility for memory trace formation. doi:10.1126/science.adg9982
  183. Wang, J., Telese, F., Tan, Y., et al. (2015). LSD1n is an H4K20 demethylase regulating memory formation via transcriptional elongation control. doi:10.1038/nn.4069
  184. Dai, J., Aoto, J., & Südhof, T. C. (2019). Alternative splicing of presynaptic neurexins differentially controls postsynaptic NMDA and AMPA receptor responses. doi:10.1016/j.neuron.2019.03.032
  185. Shi, H., Zhang, X., Weng, Y.-L., et al. (2018). m6A facilitates hippocampus-dependent learning and memory through YTHDF1. doi:10.1038/s41586-018-0666-1
  186. Peterson, L. N., Kasper, J. M., Allgaier, J. A., et al. (2025). ADAR2-mediated Q/R editing of GluA2 in homeostatic synaptic plasticity. doi:10.1126/scisignal.adr1442
  187. Joglekar, A., Prjibelski, A., Mahfouz, A., et al. (2024). Single-cell long-read sequencing-based mapping reveals specialized splicing patterns in developing and adult mouse and human brain. doi:10.1038/s41593-024-01616-4
  188. Li, Y., Zhu, M., Li, X., et al. (2025). Enhanced Protein Synthesis and Hippocampus-Dependent Memory via Inhibition of YTHDF2-Mediated m6A mRNA Degradation. doi:10.1002/advs.202514926
  189. Govindarajan, A., Israely, I., Huang, S.-Y., & Tonegawa, S. (2011). The dendritic branch is the preferred integrative unit for protein synthesis-dependent LTP. doi:10.1016/j.neuron.2010.12.008
  190. Frischknecht, R., Heine, M., Perrais, D., Seidenbecher, C. I., Choquet, D., & Gundelfinger, E. D. (2009). Brain extracellular matrix affects AMPA receptor lateral mobility and short-term synaptic plasticity. doi:10.1038/nn.2338
  191. Glykys, J., Dzhala, V., Egawa, K., et al. (2014). Local impermeant anions establish the neuronal chloride concentration. doi:10.1126/science.1245423
  192. Seidl, A. H., Rubel, E. W., & Barria, A. (2015). Tuning of Ranvier node and internode properties in myelinated axons to adjust action potential timing. doi:10.1038/ncomms9073
  193. Stringer, C., Pachitariu, M., Steinmetz, N., et al. (2019). Spontaneous behaviors drive multidimensional, brainwide activity. doi:10.1126/science.aav7893
  194. Saleem, A. B., Ayaz, A., Jeffery, K. J., Harris, K. D., & Carandini, M. (2013). Integration of visual motion and locomotion in mouse visual cortex. doi:10.1038/nn.3567
  195. Ravassard, P., Kees, A., Willers, B., et al. (2013). Multisensory control of hippocampal spatiotemporal selectivity. doi:10.1126/science.1232655
  196. Zelano, C., Jiang, H., Zhou, G., et al. (2016). Nasal respiration entrains human limbic oscillations and modulates cognitive function. doi:10.1523/JNEUROSCI.2586-16.2016
  197. Flesher, S. N., Downey, J. E., Weiss, J. M., et al. (2021). A brain-computer interface that evokes tactile sensations improves robotic arm control. doi:10.1126/science.abd0380
  198. Raut, R. V., Rosenthal, Z. P., Wang, X., et al. (2025). Arousal as a universal embedding for spatiotemporal brain dynamics. doi:10.1038/s41586-025-09544-4
  199. Guo, C., Pleiss, G., Sun, Y., & Weinberger, K. Q. (2017). On Calibration of Modern Neural Networks. PMLR 70:1321-1330
  200. Geifman, Y., & El-Yaniv, R. (2017). Selective Classification for Deep Neural Networks. NeurIPS 2017
  201. Ji, Z., et al. (2023). Survey of Hallucination in NLG. doi:10.1145/3571730
  202. Correa, J. D., Lee, S., & Bareinboim, E. (2021). Nested Counterfactual Identification. arXiv:2107.03190
  203. Gorgolewski, K. J., et al. (2016). BIDS. doi:10.1038/sdata.2016.44
  204. Pernet, C. R., et al. (2019). EEG-BIDS. doi:10.1038/s41597-019-0104-8
  205. Casali, A. G., et al. (2013). PCI. doi:10.1126/scitranslmed.3006294
  206. Chalmers, D. J. (1995). Facing up to the problem of consciousness. Journal of Consciousness Studies, 2(3), 200-219.
  207. Parfit, D. (1984). Reasons and Persons. Oxford University Press.