Evidence map›Paper›PMID 40206658›Full record

ArticleMolecular therapy. Nucleic acids2025

Correcting tau isoform ratios with a long-acting antisense oligonucleotide alleviates 4R-tauopathy phenotypes.

Kuniyuki Iwata-Endo, Kentaro Sahashi, Kaori Kawai, Yusuke Fujioka, Yohei Okada, Eri Watanabe, Nobuyuki Iwade, Minaka Ishibashi, Moniruzzaman Mohammad, Asraa Faris Aldoghachi and 10 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular therapy. Nucleic acids, 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.

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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

20 authors.

Kuniyuki Iwata-EndoMolecular Neuroscience Research Center, Shiga University of Medical Science, Otsu, Shiga 520-2192, Japan.
Kentaro SahashiDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Aichi 466-8550, Japan.
Kaori KawaiDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Aichi 466-8550, Japan.
Yusuke FujiokaMolecular Neuroscience Research Center, Shiga University of Medical Science, Otsu, Shiga 520-2192, Japan.
Yohei OkadaDepartment of Neural iPSC Research, Institute for Medical Science of Aging, Aichi Medical University, Nagakute, Aichi 480-1195, Japan.
Eri WatanabeDrug Discovery Initiative, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan.
Nobuyuki IwadeDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Aichi 466-8550, Japan.
Minaka IshibashiDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Aichi 466-8550, Japan.
Moniruzzaman MohammadMolecular Neuroscience Research Center, Shiga University of Medical Science, Otsu, Shiga 520-2192, Japan.
Asraa Faris AldoghachiMolecular Neuroscience Research Center, Shiga University of Medical Science, Otsu, Shiga 520-2192, Japan.
Dilina TuerdeDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Aichi 466-8550, Japan.
Tsuyoshi FujiwaraKNC Laboratories Co., Ltd., Kobe, Hyogo 651-2271, Japan.
Shinobu HiraiDepartment of Psychiatry and Behavioral Sciences, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo 156-8506, Japan.
Haruo OkadoDepartment of Psychiatry and Behavioral Sciences, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo 156-8506, Japan.
Masahisa KatsunoDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Aichi 466-8550, Japan.
Hirohisa WatanabeDepartment of Neurology, Fujita Health University, Toyoake, Aichi 470-1192, Japan.
Kayoko KanamitsuDrug Discovery Initiative, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan.
Masahiro NeyaKNC Laboratories Co., Ltd., Kobe, Hyogo 651-2271, Japan.
Shinsuke IshigakiMolecular Neuroscience Research Center, Shiga University of Medical Science, Otsu, Shiga 520-2192, Japan.
Gen SobueAichi Medical University, Nagakute, Aichi 480-1195, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tau, a microtubule-binding protein linked to tauopathies like Alzheimer's disease and frontotemporal lobar degeneration (FTLD), has 3-repeat (3R) and 4-repeat (4R) isoforms. Accumulation of the 4R-tau is associated with FTLD, progressive supranuclear palsy (PSP), and cortico-basal degeneration (CBD). We previously showed that a loss of fused in sarcoma (FUS) or splicing factor, proline- and glutamine-rich (SFPQ) promoted 4R-tau accumulation, which induced FTLD-like behaviors and neurodegeneration in mice. Here, we developed antisense oligonucleotides (ASOs) modified with 2'-

Indexed as

4R-tauASOENAFTLDMT: Oligonucleotides: Therapies and ApplicationsPSPsplicingtautauopathies

Identifiers

PMID40206658
PMCPMC11979468

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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.