Alzheimer's disease (AD) is the leading cause of dementia globally, characterized by cognitive impairment and mental symptoms. The pathogenesis of AD remains unclear, but mitochondrial dysfunction plays a significant role. Mitochondrial impairment involves decreased activity of multiple complexes, disturbed fusion and fission, and increased reactive oxygen species (ROS). This impairment affects energy production, calcium signaling, and glucose metabolism, leading to neuronal damage and cognitive decline. Oxidative stress, caused by increased ROS production, is a key factor in AD pathology. Recent studies suggest that targeting mitochondria with drugs such as metformin, antioxidants like MitoQ, and inhibitors of mitochondrial complex I can improve mitochondrial function and prevent cognitive decline. Lifestyle modifications, including physical activity and diet, also show promise in improving mitochondrial health and reducing AD risk. Further research is needed to develop effective treatments for AD, focusing on understanding and targeting mitochondrial dysfunction.Alzheimer's disease (AD) is the leading cause of dementia globally, characterized by cognitive impairment and mental symptoms. The pathogenesis of AD remains unclear, but mitochondrial dysfunction plays a significant role. Mitochondrial impairment involves decreased activity of multiple complexes, disturbed fusion and fission, and increased reactive oxygen species (ROS). This impairment affects energy production, calcium signaling, and glucose metabolism, leading to neuronal damage and cognitive decline. Oxidative stress, caused by increased ROS production, is a key factor in AD pathology. Recent studies suggest that targeting mitochondria with drugs such as metformin, antioxidants like MitoQ, and inhibitors of mitochondrial complex I can improve mitochondrial function and prevent cognitive decline. Lifestyle modifications, including physical activity and diet, also show promise in improving mitochondrial health and reducing AD risk. Further research is needed to develop effective treatments for AD, focusing on understanding and targeting mitochondrial dysfunction.