Experimental neurologyOct 20, 2026

How exercise training may improve energy control in the memory area of the brain in Alzheimer's disease

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Oct 21, 2026

Abstract

Exercise training is associated with changes in hippocampal mitochondrial function and cognitive outcomes in Alzheimer's disease models.

Hippocampal mitochondrial dysfunction in Alzheimer's disease includes impaired processes related to energy production and cellular health.
Twenty-one studies were reviewed, examining various exercise modalities like running and swimming over periods from 4 weeks to 8 months.
Exercise training is linked to improved markers of mitochondrial health, reduced oxidative stress, and decreased levels of amyloid-β and tau proteins.
Cognitive benefits, such as enhanced spatial learning and memory, were observed alongside mitochondrial changes.
Most studies focused on static markers, limiting insights into dynamic mitochondrial function.
The findings are constrained by heterogeneity among studies and unclear risk of bias in several cases.

Simplified

Alzheimer's disease (AD) is associated with hippocampal mitochondrial dysfunction, including impaired mitophagy, biogenesis, dynamics, bioenergetics, and redox homeostasis, which may contribute to amyloid-β (Aβ) accumulation, tau pathology, and cognitive decline. This systematic review examined whether exercise training is associated with changes in hippocampal mitochondrial regulation and cognitive function in transgenic AD rodent models. Following PRISMA 2020 guidelines, PubMed, EMBASE, and Web of Science were searched up to July 2, 2026. Twenty-one studies met inclusion criteria. Exercise modalities included treadmill running, voluntary wheel running, and swimming, with durations from 4 weeks to 8 months. Risk of bias was assessed using the SYRCLE tool. Due to heterogeneity, meta-analysis was not appropriate; a narrative synthesis was performed. Exercise training was associated with changes in markers of mitophagy, biogenesis, dynamics, and function, as well as reduced oxidative stress, decreased Aβ and tau pathology, and improved spatial learning and memory. However, most studies assessed static markers rather than functional flux, and risk of bias was unclear in several domains. The evidence suggests that exercise training may be associated with hippocampal mitochondrial modulation and cognitive benefits in AD models, but conclusions are limited by heterogeneity and incomplete reporting. Further studies with functional mitochondrial assays and clear reporting of methods and results are needed.

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How exercise training may improve energy control in the memory area of the brain in Alzheimer's disease

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