Evidence map›Paper›PMID 41645754›Full record

ReviewInternational journal of molecular medicine2026

Mechanistic advances in exercise‑mediated regulation of autophagy dysfunction in Alzheimer's disease (Review).

Wei Li, Wen-Hong Wang, Yi Song, Xu-Jiong Li, Yan Li, Xia Wang, Ting-Ting Tian, Xiao Huang, Li Zhao

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in International journal of molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

9 authors.

Wei Li *Department of Exercise Physiology, Beijing Sport University, Beijing 100084, P.R. China.
Wen-Hong Wang *Key Laboratory of Bone Biomaterials and Dong Medicine‑Regulated Organoid Regeneration of Hunan Provincial Universities, Biomedical Research Institute, Hunan University of Medicine, Huaihua, Hunan 418000, P.R. China.
Yi SongDepartment of Neurosurgery, Chongqing University Three Gorges Hospital, Chongqing 404100, P.R. China.
Xu-Jiong LiDepartment of Exercise Physiology, Beijing Sport University, Beijing 100084, P.R. China.
Yan LiDepartment of Exercise Physiology, Beijing Sport University, Beijing 100084, P.R. China.
Xia WangKey Laboratory of Bone Biomaterials and Dong Medicine‑Regulated Organoid Regeneration of Hunan Provincial Universities, Biomedical Research Institute, Hunan University of Medicine, Huaihua, Hunan 418000, P.R. China.
Ting-Ting TianKey Laboratory of Bone Biomaterials and Dong Medicine‑Regulated Organoid Regeneration of Hunan Provincial Universities, Biomedical Research Institute, Hunan University of Medicine, Huaihua, Hunan 418000, P.R. China.
Xiao HuangKey Laboratory of Bone Biomaterials and Dong Medicine‑Regulated Organoid Regeneration of Hunan Provincial Universities, Biomedical Research Institute, Hunan University of Medicine, Huaihua, Hunan 418000, P.R. China.
Li ZhaoDepartment of Exercise Physiology, Beijing Sport University, Beijing 100084, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder marked by progressive cognitive decline and whose pathology is closely linked to cellular autophagy dysfunction. Autophagy is a key process involved in cell clearance. Impaired autophagy can drive neuronal damage and death related to AD pathology. Therefore, targeting autophagy dysfunction has emerged as a promising therapeutic strategy. Exercise, as a non‑pharmaceutical and low‑cost intervention method, can enhance autophagy activity and alleviate AD symptoms. However, the mechanism by which it regulates autophagy in AD remains unclear. The present review summarizes evidence that exercise acts as an effective early intervention. Exercise activates key cellular signaling pathways (mammalian target of rapamycin, sirtuin 1 and adiponectin receptor 1) and regulates microRNAs (small non‑coding RNAs) and irisin (a muscle hormone) to restore normal autophagy. The present review also explores the use of exercise combined with natural products for potential synergistic therapeutic effects. This review provides insights into developing new AD prevention and management strategies by detailing how exercise corrects AD‑related autophagy dysfunction.

Indexed as

Alzheimer DiseaseAutophagyExerciseAnimalsHumansMicroRNAsSignal TransductionMicroRNAsAlzheimer's diseaseautophagy dysfunctionexercisemechanism

Identifiers

PMID41645754
PMCPMC12885598

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.