ArticleBrain and environment2026
The impact of exercise on brain mitochondrial health and its relevance to Alzheimer's disease.
Article in Brain and environment, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by memory loss, cognitive decline, and accumulation of amyloid-β (Aβ) plaques and tau neurofibrillary tangles in the brain. Mounting evidence implicates mitochondrial dysfunction as an upstream driver of AD pathogenesis, contributing to bioenergetic deficits, oxidative stress, impaired calcium homeostasis, and chronic neuroinflammation. Given the high energy demand of the brain, the preservation of mitochondrial function is critical for neuronal health. Physical exercise is recognized for its neuroprotective effects, with growing support that it may attenuate AD progression through enhancing mitochondrial quality control. This review explores how exercise influences key mitochondrial quality control processes in the brain-including mitochondrial-biogenesis, -dynamics, and mitophagy-and how these adaptations counteract AD-related pathologies. We further examine the dual role of reactive oxygen species, the impact of exercise-induced signaling molecules such as brain-derived neurotropic factor, irisin, and insulin-like growth factor 1, and the importance of cardiorespiratory fitness in fostering mitochondrial resilience. Finally, we highlight critical gaps in our understanding of how different exercise modalities uniquely affect brain mitochondria and AD pathology. Collectively, this underscores the potential of exercise as a non-pharmacological strategy to enhance brain mitochondrial health and promote cognitive resilience in aging and AD.
Indexed as
Identifiers
What Socratic holds
Registered trials
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.