Physical Exercise and Brain Mitochondrial Fitness: The Possible Role Against A lzheimer's Disease
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Exercise is one of the most effective strategies to maintain a healthy body and mind, with particular beneficial effects of exercise on promoting brain plasticity, increasing cognition and reducing the risk of cognitive decline and dementia in later life. Moreover, the beneficial effects resulting from increased physical activity occur at different levels of cellular organization, mitochondria being preferential target organelles. The relevance of this review article relies on the need to integrate the current knowledge of proposed mechanisms, focus mitochondria, to explain the protective effects of exercise that might underlie neuroplasticity and seeks to synthesize these data in the context of exploring exercise as a feasible intervention to delay cognitive impairment associated with neurodegenerative conditions, particularly Alzheimer disease.
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Given the similarity in mitochondrial dysfunction observed in obesity, type 2 diabetes, and AD, it is reasonable to hypothesize that lifestyle interventions, if implemented in midlife or earlier, may protect against the mitochondrial dysfunction evident in AD.
“Given the similarity in mitochondrial dysfunction observed in obesity, type 2 diabetes, and AD [184,185,186,187], it is reasonable to hypothesize that these lifestyle interventions, if implemented in midlife or earlier, may protect against the mitochondrial dysfunction evident in AD.”
From Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease (2020) · cites this paper as [184]
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Mitochondrial Dysfunction and Oxidative Stress in Alzheimer’s Disease
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Exercise and mitochondrial health
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- Authors
- Bernardo, T. C., Marques‐Aleixo, I., Beleza, J., Oliveira, P. J., Ascensão, A., & Magalhães, J.
- Affiliations
- Universidade do Porto (PT)
- Biocant – Associação de Transferência de Tecnologia (PT)
- Venue
- Brain Pathology
- Publisher
- Wiley
- Published
- 2016-09
- Volume
- 26
- Issue
- 5
- Pages
- 648-663
- ISSN
- 1015-6305 (ISSN-L)
- 1750-3639
- PMC
- PMC8029062
- OpenAlex
- W2471606802
- Cited by
- 108
- References
- 248
- Citations by year
- 2026: 9 · 2025: 13 · 2024: 13 · 2023: 9 · 2022: 14 · 2021: 11 · 2020: 11 · 2019: 17 · 2018: 5 · 2017: 3 · 2016: 3
- FWCI
- 0.83
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Brain Pathology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Portuguese Foundation for Science and Technology (FCT) (POCI-01-0145-FEDER-016690 - PTDC/DTP-DES/7087/2014)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Physiology › Physical Activity and Health
- Keywords
- physical activity, mitochondrial fitness, Alzheimer's disease, neuroprotection, neuroplasticity, cognitive decline, dementia, neurodegeneration, mitochondrial function, exercise intervention
- MeSH terms
- Alzheimer Disease, Animals, Brain, Exercise Therapy, Humans, Mitochondria, Exercise, tau Proteins, Mitochondrial Diseases
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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