Evidence map›Paper›PMID 32280029›Full record

ArticleNeurobiology of aging2020

Tau pathology in early Alzheimer's disease is linked to selective disruptions in neurophysiological network dynamics.

Ece Kocagoncu, Andrew Quinn, Azadeh Firouzian, Elisa Cooper, Andrea Greve, Roger Gunn, Gary Green, Mark W Woolrich, Richard N Henson, Simon Lovestone and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Neurobiology of aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Tracking electrophysiological signatures of Alzheimer's disease: a systematic review of multimodal studies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Pooled it
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 1 country.

Ece KocagoncuDepartment of Clinical Neurosciences, University of Cambridge, Cambridge, UK; MRC Cognition and Brain Sciences Unit, University of Cambridge, Cambridge, UK. Electronic address: ek390@cam.ac.uk.
Andrew QuinnOxford Centre for Human Brain Activity, Wellcome Centre for Integrative Neuroimaging, University of Oxford, Oxford, UK; Department of Psychiatry, University of Oxford, Oxford, UK.
Azadeh FirouzianInvicro LLC, London, UK.
Elisa CooperMRC Cognition and Brain Sciences Unit, University of Cambridge, Cambridge, UK.
Andrea GreveMRC Cognition and Brain Sciences Unit, University of Cambridge, Cambridge, UK.
Roger GunnInvicro LLC, London, UK; Department of Medicine, Imperial College London, London, UK; Department of Engineering Science, University of Oxford, Oxford, UK.
Gary GreenDepartment of Psychology, University of York, York, UK.
Mark W WoolrichOxford Centre for Human Brain Activity, Wellcome Centre for Integrative Neuroimaging, University of Oxford, Oxford, UK; Department of Psychiatry, University of Oxford, Oxford, UK.
Richard N HensonMRC Cognition and Brain Sciences Unit, University of Cambridge, Cambridge, UK; Department of Psychiatry, University of Cambridge, Cambridge, UK.
Simon LovestoneDepartment of Psychiatry, University of Oxford, Oxford, UK.
Deep and Frequent Phenotyping study team
James B RoweDepartment of Clinical Neurosciences, University of Cambridge, Cambridge, UK; MRC Cognition and Brain Sciences Unit, University of Cambridge, Cambridge, UK.
MRC Cognition and Brain Sciences Unit · GBUniversity of Oxford · GBInvicro (United Kingdom) · GBUniversity of York · GB

Funding

Biotechnology and Biological Sciences Research Council BB/H008217/1Department of HealthMedical Research Council MC_U105597119Medical Research Council MC_UU_00005/12Medical Research Council MR/K005464/1Medical Research Council MR/L023784/2Medical Research Council MR/N029941/1Medical Research Council SUAG/004 RG91365Medical Research Council SUAG/010 RG91365Wellcome Trust 103838Wellcome Trust 106183/Z/14/ZWellcome Trust 203139/Z/16/Z
6 · The paper itself

Abstract

Understanding the role of Tau protein aggregation in the pathogenesis of Alzheimer's disease is critical for the development of new Tau-based therapeutic strategies to slow or prevent dementia. We tested the hypothesis that Tau pathology is associated with functional organization of widespread neurophysiological networks. We used electro-magnetoencephalography with [

Indexed as

CognitionProtein Aggregation, PathologicalSynaptic TransmissionAgedAged, 80 and overAlzheimer DiseaseFemaleHumansMagnetoencephalographyMaleMiddle AgedMolecular ImagingOccipital LobeParietal LobePositron-Emission Tomographytau Proteinstau ProteinsAlzheimer's diseaseConnectivityGraph theoryMEGPETTau

Identifiers

PMID32280029
PMCPMC7269692
OpenAlexW3011855277

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.