Evidence map›Paper›PMID 42192197›Full record

ArticleNature neuroscience2026

Microglial mitochondria transfer to astrocytes via GPNMB-enriched extracellular vesicles alleviates cognitive deficits in tauopathy mice.

Chensi Liang, Yulan Zhou, Kai Zhuang, Shuzhong Wang, Li Zhong, Dan Can, Aiyu Lei, Huifang Li, Jie Zhang, Lige Leng

Abstract read
PubMed Publisher
In one paragraph

Article in Nature neuroscience, 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. Review
  2. Review
  3. Article
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

10 authors.

Chensi LiangFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Department of Pediatrics, Women and Children's Hospital, School of Medicine, Xiamen University, Xiamen, China.
Yulan ZhouFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Department of Pediatrics, Women and Children's Hospital, School of Medicine, Xiamen University, Xiamen, China.
Kai ZhuangFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Department of Pediatrics, Women and Children's Hospital, School of Medicine, Xiamen University, Xiamen, China.
Shuzhong WangFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Department of Pediatrics, Women and Children's Hospital, School of Medicine, Xiamen University, Xiamen, China.
Li ZhongFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Department of Pediatrics, Women and Children's Hospital, School of Medicine, Xiamen University, Xiamen, China.
Dan CanFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Department of Pediatrics, Women and Children's Hospital, School of Medicine, Xiamen University, Xiamen, China.
Aiyu LeiFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Department of Pediatrics, Women and Children's Hospital, School of Medicine, Xiamen University, Xiamen, China.
Huifang LiFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Department of Pediatrics, Women and Children's Hospital, School of Medicine, Xiamen University, Xiamen, China.
Jie ZhangFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Department of Pediatrics, Women and Children's Hospital, School of Medicine, Xiamen University, Xiamen, China. jiezhang@xmu.edu.cn.ORCID http://orcid.org/0000-0003-1040-5848
Lige LengFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Department of Pediatrics, Women and Children's Hospital, School of Medicine, Xiamen University, Xiamen, China. lenglige@xmu.edu.cn.ORCID http://orcid.org/0000-0002-4288-4743

Funding

Natural Science Foundation of Fujian Province (Fujian Provincial Natural Science Foundation) 2024J010001 to LL.
6 · The paper itself

Abstract

Alzheimer's disease (AD) is an irreversible neurodegenerative disease characterized by cognitive decline. The precise molecular mechanisms that underlie the pathogenesis of AD remain elusive. Here we show that glycoprotein nonmetastatic melanoma protein B (GPNMB) is produced by microglia and transferred to astrocytes through extracellular vesicles (EVs) in PS19 tau pathology mice. Tau is cleaved in microglia to generate N-terminal fragments that form a complex on mitochondria with Parkin/Nix and GPNMB, promoting the secretion of EVs containing mitochondria. Functional mitochondria transferred to astrocytes via EVs markedly improve astrocytic functions and attenuate the cognitive impairments and pathogenic features in PS19 mice. By contrast, microglial GPNMB deficiency eliminates mitochondrial EV secretion and mitochondrial transfer to astrocytes, thereby impairing astrocytic functions and exacerbating cognitive impairment in PS19-CcKO (CX3CR1 cre Gpnmb floxp) mice. GPNMB-enriched EVs from PS19 mice alleviate the pathological phenotypes of PS19 mice, offering potential insights for AD treatment.

Indexed as

AstrocytesCognitive DysfunctionExtracellular VesiclesEye ProteinsMembrane GlycoproteinsMicrogliaMitochondriaTauopathiesAnimalsHumansMaleMiceMice, TransgenicEye ProteinsGpnmb protein, mouseMembrane Glycoproteins

Identifiers

PMID42192197

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.