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Record W2915574395 · doi:10.1101/555821

Spread of pathological tau proteins through communicating neurons in human Alzheimer’s disease

2019· preprint· en· W2915574395 on OpenAlexafffund
Jacob W. Vogel, Yasser Iturria‐Medina, Olof Strandberg, Ruben Smith, Alan C. Evans, Oskar Hansson

Bibliographic record

VenuebioRxiv (Cold Spring Harbor Laboratory) · 2019
Typepreprint
Languageen
FieldMedicine
TopicAlzheimer's disease research and treatments
Canadian institutionsMcGill UniversityMontreal Neurological Institute and Hospital
FundersNational Institute on AgingNational Institute of Biomedical Imaging and BioengineeringCanadian Institutes of Health ResearchParkinsonfondenNational Institutes of HealthLudmer Centre for Neuroinformatics and Mental HealthH. Lundbeck A/SKnut och Alice Wallenbergs StiftelseServierVetenskapsrådetEisaiLunds UniversitetGovernment of CanadaNorthern California Institute for Research and EducationPfizerBiogenBioClinicaAustralian GovernmentF. Hoffmann-La RocheUniversity of Southern CaliforniaNovartis Pharmaceuticals CorporationGenentechMarcus och Amalia Wallenbergs minnesfondAlzheimer's Disease Neuroimaging InitiativeEli Lilly and CompanyU.S. Department of DefenseMeso Scale DiagnosticsAvid RadiopharmaceuticalsParkinson Research FoundationBristol-Myers SquibbAlzheimer's AssociationFoundation for the National Institutes of Health
KeywordsNeuroscienceNeurodegenerationAmyloid (mycology)Human Connectome ProjectPathologicalTau pathologyHuman brainConnectomeDiseaseAlzheimer's diseasePsychologyBiologyPathologyFunctional connectivityMedicine

Abstract

fetched live from OpenAlex

Abstract Tau is one of the two pathological hallmarks of Alzheimer’s disease, and bears a much closer relationship to local neurodegeneration and cognitive impairment than the other hallmark, β -amyloid. Cell and rodent models have shown evidence that tau spreads from cell to cell through anatomical neuronal connections, and that this process is facilitated by the presence of β -amyloid. We test this hypothesis in humans by using an epidemic spreading model (ESM) to simulate the spread of tau over human neuronal connections, and we compare the simulated pattern of progression to the observed pattern measured in the brains of 312 individuals on the Alzheimer’s disease spectrum, using PET. Fitting our model, we found that the majority of variance in the overall pattern of tau progression could be explained by diffusion of an agent through the human connectome, measured using either functional connectivity or diffusion tractography. These models far exceeded chance, and outperformed models testing the extracellular spread of tau over Euclidian space. Surprisingly, the ESM predicted the spatial patterns of tau irrespective of whether subjects demonstrated evidence for brain β -amyloid. In addition, in β -amyloid-positive subjects only, regions with greater amyloid burden showed greater tau than predicted by connectivity patterns, suggesting a role of amyloid in accelerating the spread of tau in certain isocortical regions. Altogether, our results provide strong evidence that tau spreads through neuronal communication pathways even in normal aging, and that this process is accelerated by the presence of brain β -amyloid.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame distilled prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: codex-gemma-dda1882f352aValidation status: machine_predicted_unvalidated
Candidate categoriesMeta-epidemiology (narrow)
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Observational · Consensus signal: Observational
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.108
Threshold uncertainty score1.000

Codex and Gemma teacher scores by category

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0010.001
Meta-epidemiology (broad)0.0010.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0010.001
Research integrity0.0000.001
Insufficient payload (model declined to judge)0.0000.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.058
GPT teacher head0.316
Teacher spread0.258 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one teacher head, not a consensus.

Study designObservational
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations56
Published2019
Admission routes2
Has abstractyes

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