Evidence map›Paper›PMID 40276591›Full record

ArticleAging brain2025

Tau aggregation induces cell death in iPSC-derived neurons.

Hirokazu Tanabe, Sumihiro Maeda, Etsuko Sano, Norio Sakai, Setsu Endoh-Yamagami, Hideyuki Okano

Abstract read
In one paragraph

Article in Aging brain, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. STAT4-dependent regulation of neuroinflammation in atherosclerosis.bioRxiv : the preprint server for biology · 2026
    Article
  5. Article
  6. Review
  7. Review
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

6 authors.

Hirokazu TanabeFUJIFILM Corporation, Bio Science & Engineering Laboratories, Kanagawa, Japan.
Sumihiro MaedaDepartment of Physiology, Keio University School of Medicine, Tokyo, Japan.
Etsuko SanoKeio University Regenerative Medicine Research Center, Kanagawa, Japan.
Norio SakaiDepartment of Molecular and Pharmacological Neuroscience, Graduate School of Biomedical & Health Sciences Hiroshima University, Hiroshima, Japan.
Setsu Endoh-YamagamiFUJIFILM Corporation, Bio Science & Engineering Laboratories, Kanagawa, Japan.
Hideyuki OkanoDepartment of Physiology, Keio University School of Medicine, Tokyo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Abnormal accumulation of tau proteins in the brain is a hallmark of neurodegenerative diseases such as Alzheimer's disease and is closely linked with neuronal cell death. Tau accumulation is a prominent therapeutic target for Alzheimer's disease, since tau accumulation correlates well with the disease progression, and tau-targeting drugs hold potentials to halt the disease progression. Given the differential response of human and mouse neuronal cells, there is a critical need for a human cellular platform to quickly screen for tau-related neurodegenerative disease therapeutics. However, inducing rapid, tau-dependent neuronal cell death in human models remains challenging. In this study, we established a human cellular model capable of inducing tau aggregation-dependent neuronal cell death within two weeks via tau overexpression. Additionally, we demonstrated the neuroprotective efficacy of known tau-targeting compounds within this system. These findings suggest that our cellular model recapitulates the molecular pathogenesis of tau-induced neurodegeneration and could serve as a valuable platform for drug screening in tauopathies.

Indexed as

AggregationiPSCNeuronal cell deathOverexpressionTau

Identifiers

PMID40276591
PMCPMC12018045

What OpenQuestion holds

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Registered trials

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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.