Evidence map›Paper›PMID 34415486›Full record

ReviewMolecular neurobiology2021

The Beneficial Role of Exercise on Treating Alzheimer's Disease by Inhibiting β-Amyloid Peptide.

Zi-Xuan Tan, Fang Dong, Lin-Yu Wu, Ya-Shuo Feng, Feng Zhang

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 12% of its field
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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  4. Aerobic exercise significantly altersJournal of Alzheimer's disease : JAD · 2026
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  20. Disentangling Mitochondria in Alzheimer's Disease.International journal of molecular sciences · 2021
    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

5 authors at 1 institution in 1 country.

Zi-Xuan TanDepartment of Rehabilitation Medicine, The Third Hospital of Hebei Medical University, No. 139 Ziqiang Road, Shijiazhuang, Hebei, 050051, People's Republic of China.
Fang DongDepartment of Clinical Laboratory Medicine, The Third Hospital of Hebei Medical University, Shijiazhuang, 050051, People's Republic of China.
Lin-Yu WuDepartment of Rehabilitation Medicine, The Third Hospital of Hebei Medical University, No. 139 Ziqiang Road, Shijiazhuang, Hebei, 050051, People's Republic of China.
Ya-Shuo FengDepartment of Rehabilitation Medicine, The Third Hospital of Hebei Medical University, No. 139 Ziqiang Road, Shijiazhuang, Hebei, 050051, People's Republic of China.
Feng ZhangDepartment of Rehabilitation Medicine, The Third Hospital of Hebei Medical University, No. 139 Ziqiang Road, Shijiazhuang, Hebei, 050051, People's Republic of China. ydsyzf@hebmu.edu.cn.ORCID http://orcid.org/0000-0002-7845-7970
Hebei Medical University · CN

Funding

National Natural Science Foundation of China 82072531
6 · The paper itself

Abstract

Alzheimer's disease (AD) is associated with a very large burden on global healthcare systems. Thus, it is imperative to find effective treatments of the disease. One feature of AD is the accumulation of neurotoxic β-amyloid peptide (Aβ). Aβ induces multiple pathological processes that are deleterious to nerve cells. Despite the development of medications that target the reduction of Aβ to treat AD, none has proven to be effective to date. Non-pharmacological interventions, such as physical exercise, are also being studied. The benefits of exercise on AD are widely recognized. Experimental and clinical studies have been performed to verify the role that exercise plays in reducing Aβ deposition to alleviate AD. This paper reviewed the various mechanisms involved in the exercise-induced reduction of Aβ, including the regulation of amyloid precursor protein cleaved proteases, the glymphatic system, brain-blood transport proteins, degrading enzymes and autophagy, which is beneficial to promote exercise therapy as a means of prevention and treatment of AD and indicates that exercise may provide new therapeutic targets for the treatment of AD.

Indexed as

ExerciseAlzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsAutophagyBlood-Brain BarrierBrain-Derived Neurotrophic FactorCarrier ProteinsDisease Models, AnimalFibronectinsGlymphatic SystemHumansMembrane MicrodomainsMiceNerve Tissue ProteinsAmyloid beta-PeptidesAmyloid beta-Protein PrecursorBrain-Derived Neurotrophic FactorCarrier ProteinsFibronectinsFNDC5 protein, humanNerve Tissue ProteinsPeptide HydrolasesPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaSirtuin 1Alzheimer’s diseaseAmyloid precursor proteinExerciseβ-Amyloid peptide

Identifiers

PMID34415486
OpenAlexW3195880618

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.