Alzheimer's disease (AD) is a progressive neurodegenerative disorder, and its prevalence is rising in tandem with the aging of the population. The primary pathological characteristics of AD encompass the aggregation of amyloid β-protein and the formation of neurofibrillary tangles resulting from the hyperphosphorylation of tau protein. The dynamic equilibrium between mitochondrial fission and fusion is fundamental for maintaining neuronal energy metabolism and cellular homeostasis, and the disruption of this equilibrium represents a key pathological event in the early stages of AD. Aberrant mitochondrial dynamics play a critical role in the pathogenesis of AD, predominantly characterized by enhanced mitochondrial fission and impaired fusion, which subsequently induce cell death and neuronal injury. This review delves into the pathological mechanisms of mitochondrial fission and fusion regulated by amyloid β-protein, tau protein, APOE4, and ferroptosis, with the aim of providing novel intervention targets for the prevention and treatment of AD.