Abstract: This paper describes the study of mitochondrial dysfunction in the brain of Alzheimer's disease (AD) and provides a theoretical basis for the prevention and mitigation of AD. AD is a neurodegenerative disease. Mitochondrial dysfunction induced by Aβ deposition in mitochondria is one of its pathogenesis. Mitochondrial Aβ deposition caused the increase of mitochondrial oxidative stress, weakened the mitochondrial biogenesis, induced mitochondrial mediated apoptosis, resulting in mitochondrial quality control imbalance, and aggravated the pathological process of AD. Recent studies have focused on brain mitochondria and found that exercise can improve mitochondrial dysfunction in AD brain. The specific effects are as follows: exercise can reduce the level of oxidative stress in the brain of AD, promote mitochondrial biogenesis in the brain of AD, inhibit the excessive apoptosis of mitochondria mediated cells, maintain mitochondrial fission and fusion balance, and improve the autophagy activity of mitochondria in order to prevent and alleviate AD.