Evidence map›Paper›PMID 42455424›Full record

ArticleMolecular biomedicine2026

Higher physical activity levels mitigate synaptic protein loss and cognitive deterioration in aging and in Alzheimer's disease: a 10-year longitudinal study.

Shuiyue Quan, Xiaofeng Fu, Huimin Cai, Weiyun Zhang, Yumei Geng, Qing Tian, Ziye Ren, Yinghao Xu, Chengyu An, Jiaqi Li and 2 more

Abstract read
In one paragraph

Article in Molecular biomedicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Shuiyue QuanDepartment of Neurology and Innovation Center for Neurological Disorders, National Clinical Research Center for Geriatric Diseases, Xuanwu Hospital, Capital Medical University, 45 Changchun St., Beijing, 100053, China.
Xiaofeng FuDepartment of Neurology and Innovation Center for Neurological Disorders, National Clinical Research Center for Geriatric Diseases, Xuanwu Hospital, Capital Medical University, 45 Changchun St., Beijing, 100053, China.
Huimin CaiDepartment of Neurology and Innovation Center for Neurological Disorders, National Clinical Research Center for Geriatric Diseases, Xuanwu Hospital, Capital Medical University, 45 Changchun St., Beijing, 100053, China.
Weiyun ZhangDepartment of Neurology and Innovation Center for Neurological Disorders, National Clinical Research Center for Geriatric Diseases, Xuanwu Hospital, Capital Medical University, 45 Changchun St., Beijing, 100053, China.
Yumei GengDepartment of Neurology and Innovation Center for Neurological Disorders, National Clinical Research Center for Geriatric Diseases, Xuanwu Hospital, Capital Medical University, 45 Changchun St., Beijing, 100053, China.
Qing TianDepartment of Neurology and Innovation Center for Neurological Disorders, National Clinical Research Center for Geriatric Diseases, Xuanwu Hospital, Capital Medical University, 45 Changchun St., Beijing, 100053, China.
Ziye RenDepartment of Neurology and Innovation Center for Neurological Disorders, National Clinical Research Center for Geriatric Diseases, Xuanwu Hospital, Capital Medical University, 45 Changchun St., Beijing, 100053, China.
Yinghao XuDepartment of Neurology and Innovation Center for Neurological Disorders, National Clinical Research Center for Geriatric Diseases, Xuanwu Hospital, Capital Medical University, 45 Changchun St., Beijing, 100053, China.
Chengyu AnDepartment of Neurology and Innovation Center for Neurological Disorders, National Clinical Research Center for Geriatric Diseases, Xuanwu Hospital, Capital Medical University, 45 Changchun St., Beijing, 100053, China.
Jiaqi LiDepartment of Neurology and Innovation Center for Neurological Disorders, National Clinical Research Center for Geriatric Diseases, Xuanwu Hospital, Capital Medical University, 45 Changchun St., Beijing, 100053, China.
Wei WangDepartment of Neurology and Innovation Center for Neurological Disorders, National Clinical Research Center for Geriatric Diseases, Xuanwu Hospital, Capital Medical University, 45 Changchun St., Beijing, 100053, China. sunnywangwei@163.com.
Longfei JiaDepartment of Neurology and Innovation Center for Neurological Disorders, National Clinical Research Center for Geriatric Diseases, Xuanwu Hospital, Capital Medical University, 45 Changchun St., Beijing, 100053, China. longfei@mail.ccmu.edu.cn.ORCID http://orcid.org/0000-0003-3648-3668

Funding

Beijing Brain Initiative of the Beijing Municipal Science & Technology Commission Z201100005520016Beijing Municipal Natural Science Foundation 7202061Capital's Funds for Health Improvement and Research 2022-2-2017National Natural Science Foundation of China 82471210National Natural Science Foundation of China U24A20681STI 2030-Major Projects 2022ZD0211600STI 2030-Major Projects 2022ZD0211605
6 · The paper itself

Abstract

Synaptic degeneration is a hallmark of Alzheimer's disease (AD) and is closely linked to cognitive decline. Although physical activity (PA) can preserve synaptic integrity and cognitive function, its long-term effects during aging and AD progression remain poorly characterized. Here, we conducted a 10-year longitudinal study to investigate the effects of different PA levels on synaptic proteins and cognitive function during aging and in AD progression. The study included 231 cognitively normal older adults (preclinical AD, 116; controls, 115), who were stratified based on their PA intensity. Plasma was collected every 2 years to quantify four synaptic proteins (GAP43, neurogranin, SNAP25, and synaptotagmin 1) in neuron-derived extracellular vesicles (EVs), with concurrent cognitive assessments. The results indicated that all synaptic proteins declined over time, with a greater reduction in AD than in normal aging (P < 0.05). Synaptic protein levels did not differ between PA groups at baseline (P > 0.05), but at the 10-year follow-up, participants with higher PA had significantly greater synaptic protein levels than those with lower PA in both AD and controls (P < 0.05). Consistently, higher PA alleviated synaptic protein loss during aging (P < 0.05). Furthermore, higher PA was associated with slower cognitive decline in patients with preclinical AD (P < 0.05). Our study suggests that higher levels of PA may mitigate age- and AD-related synaptic deterioration, thereby contributing to cognitive resilience in late life.

Indexed as

AgingAlzheimer DiseaseCognitionSynapsesAgedAged, 80 and overDisease ProgressionFemaleHumansLongitudinal StudiesMaleAgingAlzheimer’s diseaseLongitudinalPhysical activitySynaptic protein

Identifiers

PMID42455424
PMCPMC13373128

What Socratic holds

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LicenceCC BY
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Registered trials

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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 Socratic graph.