Abstract: Alzheimer's disease (AD) is a complex neurodegenerative disorder, and its pathological mechanisms are not yet fully understood. In recent years, mitochondrial dysfunction has been recognized as one of the important pathological features of AD. As the central hub of intracellular energy metabolism, mitochondria maintain ATP homeostasis through the tricarboxylic acid cycle and oxidative phosphorylation under physiological conditions, and they are involved in important physiological processes. However, under the pathological state of AD, mitochondrial function undergoes statistically significant changes, characterized by bioenergetic metabolism imbalance, impaired mitophagy, abnormal dynamics (including excessive fission and fusion defects), and excessive production of mitochondrial reactive oxygen species. Moreover, abnormal interactions between mitochondria and the endoplasmic reticulum disrupt cellular homeostasis, thereby significantly accelerating neuronal degeneration by exacerbating the pathological processes of AD. This article systematically reviews the core pathological features of AD, focusing on the physiological functions of mitochondria and their dynamic changes during the pathological progression of AD. Finally, this article summarizes the anti-AD therapeutic strategies that regulate mitochondrial function, including small molecule drugs and natural products, providing new ideas and potential solutions for the treatment of AD.