Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive impairment and mental symptoms, being the most common cause of dementia globally. The pathogenesis of AD remains unclear, with key features including amyloid beta (Aβ) plaques, hyperphosphorylated tau protein, and neuronal loss. Mitochondrial dysfunction plays a critical role in AD pathogenesis, contributing to oxidative stress, impaired energy metabolism, and synaptic loss. Mitochondrial impairment is associated with reduced activity of multiple complexes, disrupted fusion and fission processes, and increased reactive oxygen species (ROS). Mitochondrial transport is also impaired in AD, leading to synaptic loss and cognitive decline. Mitochondrial dysfunction affects amyloid precursor protein (APP) production, APP cleavage, and Aβ accumulation. It also stimulates other molecular changes, such as impaired tau phosphorylation and inflammation. Insulin signaling disruption impairs mitochondrial Aβ removal, exacerbating AD. Recent studies suggest that metformin and antioxidants like MitoQ, SS-31, SkQ, MitoApo, MitoTEMPO, and MitoVitE may improve mitochondrial function and prevent cognitive decline. Mitochondrial division inhibitor-1 and ceramide may also be therapeutic options. Oxidative stress is a major contributor to AD, with ROS damaging neurons and contributing to Aβ accumulation. Antioxidants such as MitoQ and SS-31 have shown neuroprotective effects. Glucose metabolism impairment is linked to AD, with insulin resistance and glucose hypometabolism playing a role. Mitochondria-targeted therapies, including metformin, MitoQ, and other antioxidants, are being explored for their potential to treat AD. Lifestyle modifications, such as exercise and a Mediterranean diet, may also help prevent or slow AD progression. Research indicates that exercise improves mitochondrial biogenesis, reduces oxidative stress, and enhances cognitive function. Dietary factors, including long-chain polyunsaturated fatty acids and calorie restriction, may also have protective effects. In summary, mitochondrial dysfunction is a key factor in AD pathogenesis, and targeting mitochondrial function through various therapies may offer new treatment options. Further research is needed to develop effective and safe treatments for AD.Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive impairment and mental symptoms, being the most common cause of dementia globally. The pathogenesis of AD remains unclear, with key features including amyloid beta (Aβ) plaques, hyperphosphorylated tau protein, and neuronal loss. Mitochondrial dysfunction plays a critical role in AD pathogenesis, contributing to oxidative stress, impaired energy metabolism, and synaptic loss. Mitochondrial impairment is associated with reduced activity of multiple complexes, disrupted fusion and fission processes, and increased reactive oxygen species (ROS). Mitochondrial transport is also impaired in AD, leading to synaptic loss and cognitive decline. Mitochondrial dysfunction affects amyloid precursor protein (APP) production, APP cleavage, and Aβ accumulation. It also stimulates other molecular changes, such as impaired tau phosphorylation and inflammation. Insulin signaling disruption impairs mitochondrial Aβ removal, exacerbating AD. Recent studies suggest that metformin and antioxidants like MitoQ, SS-31, SkQ, MitoApo, MitoTEMPO, and MitoVitE may improve mitochondrial function and prevent cognitive decline. Mitochondrial division inhibitor-1 and ceramide may also be therapeutic options. Oxidative stress is a major contributor to AD, with ROS damaging neurons and contributing to Aβ accumulation. Antioxidants such as MitoQ and SS-31 have shown neuroprotective effects. Glucose metabolism impairment is linked to AD, with insulin resistance and glucose hypometabolism playing a role. Mitochondria-targeted therapies, including metformin, MitoQ, and other antioxidants, are being explored for their potential to treat AD. Lifestyle modifications, such as exercise and a Mediterranean diet, may also help prevent or slow AD progression. Research indicates that exercise improves mitochondrial biogenesis, reduces oxidative stress, and enhances cognitive function. Dietary factors, including long-chain polyunsaturated fatty acids and calorie restriction, may also have protective effects. In summary, mitochondrial dysfunction is a key factor in AD pathogenesis, and targeting mitochondrial function through various therapies may offer new treatment options. Further research is needed to develop effective and safe treatments for AD.