Alzheimer's disease is a neurodegenerative disease that affects cognitive function. Recent studies have shown that mitochondrial dysfunction plays an important role in its pathological process. The mitochondrial fusion protein Mfn2 plays a crucial role in maintaining mitochondrial function and cellular health. The aim of this study is to explore the molecular structure of mitochondrial fusion protein Mfn2 and its role in Alzheimer's disease, combined with the effects of exercise assisted regulation, to evaluate its potential in alleviating symptoms. By constructing a brain model of Alzheimer's disease, conducting pathological analysis and molecular dynamics simulations, we aim to explore the relationship between the disease and mitochondrial function. Analyze the molecular structure of Mfn2, study its role in normal and pathological states, and evaluate its impact on Mfn2 and mitochondrial function through exercise intervention. The study demonstrated the typical pathological features of Alzheimer's disease and confirmed the relationship between mitochondrial dysfunction and disease progression. The structural analysis of mitochondrial fusion protein Mfn2 indicates its importance in promoting mitochondrial fusion. Exercise intervention significantly increased the expression of Mfn2 and improved mitochondrial function, further alleviating pathological changes associated with Alzheimer's disease.