Evidence map›Paper›PMID 40914755›Full record

ArticleMolecular psychiatry2026

Astrocytic Mettl14 depletion enhances cognitive function by attenuating astrogliosis via the DUSP1/MAPK pathway in APP/PS1 mice: targeting neuroinflammation in Alzheimer's disease.

Yan Teng, Jianli Xu, Shu He, Jin Yi, Manjun Li, Qin Tang, Xingmin Chen, Fan Wei, Yanzhuo Liu, Haisong Jiang and 6 more

Abstract read
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In one paragraph

Article in Molecular psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  2. Article
  3. 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

16 authors.

Yan Teng *Institute of Neurology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China.ORCID http://orcid.org/0000-0002-8850-251X
Jianli Xu *Institute of Neurology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China.
Shu He *School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China.
Jin YiSchool of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China.
Manjun LiSchool of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China.
Qin TangSchool of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China.
Xingmin ChenSchool of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China.
Fan WeiSchool of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China.
Yanzhuo LiuSchool of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China.
Haisong JiangSchool of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China.
Yang XiangInstitute of Neurology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China.
Jia-Ling ZhaoInstitute of Neurology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China.
Jing YangInstitute of Neurology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China.
Weidong LeInstitute of Neurology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China. wdle@sibs.ac.cn.
Min ZhengSchool of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China. zhengmin625@uestc.edu.cn.
Lu YangInstitute of Neurology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China. lyang@uestc.edu.cn.ORCID http://orcid.org/0000-0001-9144-3234

Funding

Department of Science and Technology of Sichuan Province (Sichuan Provincial Department of Science and Technology) 2022YFS0597National Natural Science Foundation of China (National Science Foundation of China) 81601125National Natural Science Foundation of China (National Science Foundation of China) 82271524National Natural Science Foundation of China (National Science Foundation of China) 82302630
6 · The paper itself

Abstract

Alzheimer's disease (AD), a leading cause of dementia, represents a critical unmet global medical need. While the precise mechanisms underlying AD pathogenesis remain elusive, increasing evidence underscores the pivotal role of neuroinflammation in driving cognitive impairment. N6-methyladenosine (m6A), an epigenetic modification regulating RNA metabolism, has been found to be dysregulated in AD. In this study, we used a Mettl14 conditional knockout APP/PS1 mouse model (AD-cKO mice) to investigate the effects of modulating astrocytic m6A levels on AD progression. Our comprehensive histological, biochemical, and transcriptomic analyses revealed that AD-cKO mice exhibited enhanced cognitive function, along with decreased astrogliosis and reduced neuroinflammation when compared to APP/PS1 control mice. Based on the conjoint analysis of MeRIP-seq and RNA-seq data, our mechanistic studies further demonstrated that the loss of Mettl14 in astrocytes significantly affected the expression of DUSP1, a negative regulator of inflammation, to mitigate MAPK signaling. These findings suggest that targeting m6A regulators, such as Mettl14, may represent a promising therapeutic strategy to control neuroinflammation in AD progression. This study also highlights the broader potential of epigenetic modulation as a novel approach for treating AD. This graphic abstract illustrates the impact of Mettl14-mediated m6A modification on Alzheimer's disease (AD) pathogenesis. Alzheimer's disease, a leading cause of dementia, involves significant neuroinflammation. The study utilizes a Mettl14 conditional knockout APP/PS1 mouse model (AD-cKO mice) to investigate the role of m6A modification in astrocytes, the findings suggest that targeting m6A regulators like Mettl14 offers potential therapeutic benefits for controlling neuroinflammation in AD.

Indexed as

Alzheimer DiseaseDual Specificity Phosphatase 1GliosisMethyltransferasesAdenosineAmyloid beta-Protein PrecursorAnimalsAstrocytesCognitionCognitive DysfunctionDisease Models, AnimalInflammationMaleMAP Kinase Signaling SystemMiceMice, Inbred C57BLAdenosineAmyloid beta-Protein PrecursorDual Specificity Phosphatase 1Dusp1 protein, mouseMethyltransferasesMettl14 protein, mouseN-methyladenosinePresenilin-1

Identifiers

PMID40914755

What Socratic holds

Textmetadata
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 Socratic graph.