Evidence map›Paper›PMID 33632820›Full record

ReviewScience (New York, N.Y.)2021

Tau: Enabler of diverse brain disorders and target of rapidly evolving therapeutic strategies.

Che-Wei Chang, Eric Shao, Lennart Mucke

Open access · greenAbstract readReview
In one paragraph

Review in Science (New York, N.Y.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 138 papers.

0numbers the graph read from it
0cells of the map it votes in
138citing papers in PubMed
22.3field-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

138 citing papers in PubMed, 246 citations in OpenAlex.

  1. Trial
  2. Article
  3. Shared genetic architecture between DTI-ALPS traits and neurodegenerative diseases.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  4. Article
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  6. Patient-derived forebrain cortical organoids reveal biphasic tau-MAP6-microtubule axis dysfunction in tauopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  7. Review
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  11. Review
  12. Article
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  15. Article
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  20. Article

78 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.

Che-Wei ChangGladstone Institute of Neurological Disease, Gladstone Institutes, San Francisco, CA 94158, USA.ORCID https://orcid.org/0000-0003-1043-581X
Eric ShaoGladstone Institute of Neurological Disease, Gladstone Institutes, San Francisco, CA 94158, USA.ORCID https://orcid.org/0000-0001-5307-8264
Lennart MuckeGladstone Institute of Neurological Disease, Gladstone Institutes, San Francisco, CA 94158, USA. lennart.mucke@gladstone.ucsf.edu.ORCID https://orcid.org/0000-0001-6256-9559
Gladstone Institutes · US

Funding

Therapeutic Potential and Mechanisms of Tau Reduction in Autism ModelsR01MH115679 · NIMH · J. DAVID GLADSTONE INSTITUTES · PI MUCKE, LENNART · 2018 to 2022
$3.6M
Identification and Development of Tau-Lowering Small-Molecule DrugsR56AG060631 · NIA · J. DAVID GLADSTONE INSTITUTES · PI MUCKE, LENNART · 2019 to 2019
$1.7M
Effect of Aging on Efficacy of Alzheimer-focused Therapeutic StrategiesUH3NS100128 · NINDS · J. DAVID GLADSTONE INSTITUTES · PI MUCKE, LENNART · 2018 to 2020
$504k
NIA NIH HHS R56 AG060631NIMH NIH HHS R01 MH115679NINDS NIH HHS UH3 NS100128
6 · The paper itself

Abstract

Several lines of evidence implicate the protein tau in the pathogenesis of multiple brain disorders, including Alzheimer's disease, other neurodegenerative conditions, autism, and epilepsy. Tau is abundant in neurons and interacts with microtubules, but its main functions in the brain remain to be defined. These functions may involve the regulation of signaling pathways relevant to diverse biological processes. Informative disease models have revealed a plethora of abnormal tau species and mechanisms that might contribute to neuronal dysfunction and loss, but the relative importance of their respective contributions is uncertain. This knowledge gap poses major obstacles to the development of truly impactful therapeutic strategies. The current expansion and intensification of efforts to translate mechanistic insights into tau-related therapeutics should address this issue and could deliver better treatments for a host of devastating conditions.

Indexed as

AnimalsBrainBrain DiseasesHumansMicrotubulesNeuronsTauopathiestau ProteinsMAPT protein, humantau Proteins

Identifiers

PMID33632820
PMCPMC8118650
OpenAlexW3129727567

What OpenQuestion holds

Textmetadata
LicenceTDM
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.