Evidence map›Paper›PMID 32728795›Full record

ReviewActa neuropathologica2020

The physiological roles of tau and Aβ: implications for Alzheimer's disease pathology and therapeutics.

Sarah A Kent, Tara L Spires-Jones, Claire S Durrant

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Acta neuropathologica, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 242 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
242citing papers in PubMed, 2 pooled it
26.0field-weighted citation impact, top 1% 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

242 citing papers in PubMed, 2 syntheses or guidelines pooled it, 422 citations in OpenAlex.

  1. Pooled it
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  3. Article
  4. Rethinking tau-targeted therapy in Alzheimer's disease: Toward a dual biomarker strategy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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182 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Sarah A KentTranslational Neuroscience PhD Programme, Centre for Discovery Brain Sciences and the UK Dementia Research Institute, The University of Edinburgh, 1 George Square, Edinburgh, EH8 9JZ, Scotland, UK.ORCID http://orcid.org/0000-0002-8545-3724
Tara L Spires-JonesCentre for Discovery Brain Sciences and the UK Dementia Research Institute, The University of Edinburgh, 1 George Square, Edinburgh, EH8 9JZ, Scotland, UK.ORCID http://orcid.org/0000-0003-2530-0598
Claire S DurrantCentre for Discovery Brain Sciences and the UK Dementia Research Institute, The University of Edinburgh, 1 George Square, Edinburgh, EH8 9JZ, Scotland, UK. claire.durrant@ed.ac.uk.ORCID http://orcid.org/0000-0001-7552-7358
UK Dementia Research Institute · GB

Funding

European Research Council 681181Wellcome Trust
6 · The paper itself

Abstract

Tau and amyloid beta (Aβ) are the prime suspects for driving pathology in Alzheimer's disease (AD) and, as such, have become the focus of therapeutic development. Recent research, however, shows that these proteins have been highly conserved throughout evolution and may have crucial, physiological roles. Such functions may be lost during AD progression or be unintentionally disrupted by tau- or Aβ-targeting therapies. Tau has been revealed to be more than a simple stabiliser of microtubules, reported to play a role in a range of biological processes including myelination, glucose metabolism, axonal transport, microtubule dynamics, iron homeostasis, neurogenesis, motor function, learning and memory, neuronal excitability, and DNA protection. Aβ is similarly multifunctional, and is proposed to regulate learning and memory, angiogenesis, neurogenesis, repair leaks in the blood-brain barrier, promote recovery from injury, and act as an antimicrobial peptide and tumour suppressor. This review will discuss potential physiological roles of tau and Aβ, highlighting how changes to these functions may contribute to pathology, as well as the implications for therapeutic development. We propose that a balanced consideration of both the physiological and pathological roles of tau and Aβ will be essential for the design of safe and effective therapeutics.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsHumanstau ProteinsAmyloid beta-Peptidestau ProteinsMemoryMicrotubule dynamicsMyelinationSynapseTherapeuticsVasculature

Identifiers

PMID32728795
PMCPMC7498448
OpenAlexW3045897262

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.