Evidence map›Paper›PMID 39462160›Full record

ArticleBrain pathology (Zurich, Switzerland)2025

Aerobic exercise improves astrocyte mitochondrial quality and transfer to neurons in a mouse model of Alzheimer's disease.

Jiachen Cai, Yan Chen, Yuzhu She, Xiaoxin He, Hu Feng, Huaiqing Sun, Mengmei Yin, Junying Gao, Chengyu Sheng, Qian Li and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
–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

16 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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

11 authors.

Jiachen CaiJiangsu Key Laboratory of Neurodegeneration, Nanjing Medical University, Nanjing, China.
Yan ChenJiangsu Key Laboratory of Neurodegeneration, Nanjing Medical University, Nanjing, China.
Yuzhu SheJiangsu Key Laboratory of Neurodegeneration, Nanjing Medical University, Nanjing, China.
Xiaoxin HeJiangsu Key Laboratory of Neurodegeneration, Nanjing Medical University, Nanjing, China.
Hu FengJiangsu Key Laboratory of Neurodegeneration, Nanjing Medical University, Nanjing, China.
Huaiqing SunJiangsu Key Laboratory of Neurodegeneration, Nanjing Medical University, Nanjing, China.
Mengmei YinJiangsu Key Laboratory of Neurodegeneration, Nanjing Medical University, Nanjing, China.
Junying GaoJiangsu Key Laboratory of Neurodegeneration, Nanjing Medical University, Nanjing, China.
Chengyu ShengJiangsu Key Laboratory of Neurodegeneration, Nanjing Medical University, Nanjing, China.
Qian LiJiangsu Key Laboratory of Neurodegeneration, Nanjing Medical University, Nanjing, China.
Ming XiaoJiangsu Key Laboratory of Neurodegeneration, Nanjing Medical University, Nanjing, China.ORCID 0000-0001-5528-9102

Funding

National Natural Science Foundation of China 81871117National Natural Science Foundation of China 82471608Natural Science Foundation of Jiangsu Province BK20230057Natural Science Foundation of the Jiangsu Higher Education Institutions of China 23KJB310009
6 · The paper itself

Abstract

Mitochondrial dysfunction is a well-established hallmark of Alzheimer's disease (AD). Despite recent documentation of transcellular mitochondrial transfer, its role in the pathogenesis of AD remains unclear. In this study, we report an impairment of mitochondrial quality within the astrocytes and neurons of adult 5 × FAD mice. Following treatment with mitochondria isolated from aged astrocytes induced by exposure to amyloid protein or extended cultivation, cultured neurons exhibited an excessive generation of reactive oxygen species and underwent neurite atrophy. Notably, aerobic exercise enhanced mitochondrial quality by upregulating CD38 within hippocampal astrocytes of 5 × FAD mice. Conversely, the knockdown of CD38 diminished astrocytic-neuronal mitochondrial transfer, thereby abolishing the ameliorative effects of aerobic exercise on neuronal oxidative stress, β-amyloid plaque deposition, and cognitive dysfunction in 5 × FAD mice. These findings unveil an unexpected mechanism through which aerobic exercise facilitates the transference of healthy mitochondria from astrocytes to neurons, thus countering the AD-like progression.

Indexed as

Alzheimer DiseaseAstrocytesMitochondriaNeuronsADP-ribosyl Cyclase 1AerobiosisAnimalsAtrophyCells, CulturedCellular SenescenceDisease Models, AnimalHippocampusMaleMembrane GlycoproteinsMiceMice, Inbred C57BLADP-ribosyl Cyclase 1Cd38 protein, mouseMembrane GlycoproteinsAlzheimer's diseaseastrocytesCD38exercisemitochondrial transfer

Identifiers

PMID39462160
PMCPMC11961210

What OpenQuestion holds

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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.