New evidence demonstrates that mitochondrial DNA mutations accumulate progressively with age and reduce ATP production in neurons, substantially accelerating the onset of neurodegenerative diseases including Alzheimer’s and Parkinson’s. However, emerging data provides a protective pathway: aerobic exercise enhances mitochondrial antioxidant defences and slows age-related mtDNA damage accumulation. This finding offers clinically meaningful implications for disease prevention strategies. Regular physical activity increases expression of superoxide dismutase, catalase, and glutathione peroxidase—the primary enzymatic systems that neutralise reactive oxygen species generated during mitochondrial respiration. By maintaining these antioxidant defences, exercise reduces oxidative stress on mitochondrial DNA and preserves electron transport chain function. These observations suggest that structured aerobic programmes may represent an accessible, evidence-based intervention for reducing neurodegenerative disease risk across populations.
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