Evidence map›Paper›PMID 39769339›Full record

ReviewInternational journal of molecular sciences2024

Understanding the Molecular Impact of Physical Exercise on Alzheimer's Disease.

Alba Cantón-Suárez, Leticia Sánchez-Valdeón, Laura Bello-Corral, María J Cuevas, Brisamar Estébanez

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Ocular Glymphatic System: Its Modulation and Role in Intraocular Tumors.Investigative ophthalmology & visual science · 2026
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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

5 authors.

Alba Cantón-SuárezFaculty of Health Sciences, University of Leon, 24071 Leon, Spain.ORCID 0009-0000-6644-3689
Leticia Sánchez-ValdeónHealth Research Nursing Group (GREIS), University of Leon, 24071 Leon, Spain.ORCID 0000-0003-4931-4644
Laura Bello-CorralHealth Research Nursing Group (GREIS), University of Leon, 24071 Leon, Spain.ORCID 0000-0001-6656-2813
María J CuevasInstitute of Biomedicine (IBIOMED), University of León, 24071 Leon, Spain.
Brisamar EstébanezInstitute of Biomedicine (IBIOMED), University of León, 24071 Leon, Spain.ORCID 0000-0001-5034-9508

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease is one of the most common neurodegenerative diseases, characterized by a wide range of neurological symptoms that begin with personality changes and psychiatric symptoms, progress to mild cognitive impairment, and eventually lead to dementia. Physical exercise is part of the non-pharmacological treatments used in Alzheimer's disease, as it has been shown to delay the neurodegenerative process by improving the redox state in brain tissue, providing anti-inflammatory effects or stimulating the release of the brain-derived neurotrophic factor that enhances the brain structure and cognitive performance. Here, we reviewed the results obtained from studies conducted in both animal models and human subjects to comprehend how physical exercise interventions can exert changes in the molecular mechanisms underlying the pathophysiological processes in Alzheimer's disease: amyloid β-peptide pathology, tau pathology, neuroglial changes, mitochondrial dysfunction, and oxidative stress. Physical exercise seems to have a protective effect against Alzheimer's disease, since it has been shown to induce positive changes in some of the biomarkers related to the pathophysiological processes of the disease. However, additional studies in humans are necessary to address the current lack of conclusive evidence.

Indexed as

Alzheimer DiseaseExerciseOxidative StressAmyloid beta-PeptidesAnimalsBiomarkersBrainExercise TherapyHumansMitochondriatau ProteinsAmyloid beta-PeptidesBiomarkerstau ProteinsAlzheimer’s diseaseamyloid β-peptidemitochondrial dysfunctionmolecular mechanismsneurodegenerationneurogliaoxidative stressphysical activitytau protein

Identifiers

PMID39769339
PMCPMC11677557

What Socratic holds

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LicenceCC BY
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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 Socratic graph.