Evidence map›Paper›PMID 38556838›Full record

ReviewAlzheimer's & dementia : the journal of the Alzheimer's Association2024

The six brain-specific TAU isoforms and their role in Alzheimer's disease and related neurodegenerative dementia syndromes.

Sarah Buchholz, Hans Zempel

Open access · hybridAbstract readReview
In one paragraph

Review in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed
29.4field-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

86 citing papers in PubMed, 90 citations in OpenAlex.

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  17. Tau protein as a regulator of mitochondrial function and dynamics.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  18. Genetic and environmental risk factors of Parkinsonism.Journal of neural transmission (Vienna, Austria : 1996) · 2026
    Review
  19. Review
  20. Article

26 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

2 authors at 1 institution in 1 country.

Sarah BuchholzInstitute of Human Genetics, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.ORCID 0000-0002-3636-1364
Hans ZempelInstitute of Human Genetics, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.ORCID 0000-0002-7510-3077
University of Cologne · DE

Funding

Alzheimer-Forschungs-Initiative e.V. 22039German Research Foundation 491454339
6 · The paper itself

Abstract

introductionAlternative splicing of the human MAPT gene generates six brain-specific TAU isoforms. Imbalances in the TAU isoform ratio can lead to neurodegenerative diseases, underscoring the need for precise control over TAU isoform balance. Tauopathies, characterized by intracellular aggregates of hyperphosphorylated TAU, exhibit extensive neurodegeneration and can be classified by the TAU isoforms present in pathological accumulations.

methodsA comprehensive review of TAU and related dementia syndromes literature was conducted using PubMed, Google Scholar, and preprint server.

resultsWhile TAU is recognized as key driver of neurodegeneration in specific tauopathies, the contribution of the isoforms to neuronal function and disease development remains largely elusive. DISCUSSION: In this review we describe the role of TAU isoforms in health and disease, and stress the importance of comprehending and studying TAU isoforms in both, physiological and pathological context, in order to develop targeted therapeutic interventions for TAU-associated diseases. HIGHLIGHTS: MAPT splicing is tightly regulated during neuronal maturation and throughout life. TAU isoform expression is development-, cell-type and brain region specific. The contribution of TAU to neurodegeneration might be isoform-specific. Ineffective TAU-based therapies highlight the need for specific targeting strategies.

Indexed as

Alzheimer DiseaseBrainProtein Isoformstau ProteinsAlternative SplicingAnimalsDementiaHumansNeurodegenerative DiseasesTauopathiesProtein Isoformstau Proteinsalternative splicingAlzheimer's diseasegenetic tauopathyMAPTTAU isoformstauopathy

Identifiers

PMID38556838
PMCPMC11095451
OpenAlexW4393384008

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.