Mitochondrial dynamics, including fusion, fission, movement, and mitophagy, play crucial roles in maintaining neuronal function and preventing neurodegenerative diseases. Mitochondria are dynamic organelles that undergo continuous cycles of fusion and fission, enabling lipid and content exchange, and maintaining mitochondrial quality through mitophagy. Defects in these processes are associated with various neurodegenerative diseases, including Charcot-Marie-Tooth type 2A and dominant optic atrophy, which result from mitochondrial fusion defects. Major neurodegenerative diseases such as Parkinson's, Alzheimer's, and Huntington's disease also involve disruptions in mitochondrial dynamics. Manipulating mitochondrial fusion or fission can partially rescue disease phenotypes in some models. Mitochondrial fusion is essential for mitochondrial function, while fission facilitates equal segregation of mitochondria during cell division and enhances their distribution along cytoskeletal tracks. Mitophagy, the selective degradation of defective mitochondria, is crucial for maintaining mitochondrial quality. Mitochondrial motility is vital for neurons, which require mitochondria at distant sites from the cell body. Defects in fusion and fission can impair mitochondrial movement, leading to neuronal dysfunction. Mitochondrial dynamics are interdependent, with fusion and fission influencing each other and mitophagy. In Parkinson's disease, mutations in Pink1 and Parkin affect mitochondrial integrity and function, with Pink1 involved in mitochondrial fusion and Parkin in mitophagy. In Alzheimer's disease, mitochondrial dysfunction is linked to amyloid-beta accumulation and increased mitochondrial fission. In Huntington's disease, mutant huntingtin disrupts mitochondrial dynamics, leading to mitochondrial dysfunction and neurodegeneration. Overall, mitochondrial dynamics are integral to neuronal health, and understanding these processes may lead to new therapeutic strategies for neurodegenerative diseases.Mitochondrial dynamics, including fusion, fission, movement, and mitophagy, play crucial roles in maintaining neuronal function and preventing neurodegenerative diseases. Mitochondria are dynamic organelles that undergo continuous cycles of fusion and fission, enabling lipid and content exchange, and maintaining mitochondrial quality through mitophagy. Defects in these processes are associated with various neurodegenerative diseases, including Charcot-Marie-Tooth type 2A and dominant optic atrophy, which result from mitochondrial fusion defects. Major neurodegenerative diseases such as Parkinson's, Alzheimer's, and Huntington's disease also involve disruptions in mitochondrial dynamics. Manipulating mitochondrial fusion or fission can partially rescue disease phenotypes in some models. Mitochondrial fusion is essential for mitochondrial function, while fission facilitates equal segregation of mitochondria during cell division and enhances their distribution along cytoskeletal tracks. Mitophagy, the selective degradation of defective mitochondria, is crucial for maintaining mitochondrial quality. Mitochondrial motility is vital for neurons, which require mitochondria at distant sites from the cell body. Defects in fusion and fission can impair mitochondrial movement, leading to neuronal dysfunction. Mitochondrial dynamics are interdependent, with fusion and fission influencing each other and mitophagy. In Parkinson's disease, mutations in Pink1 and Parkin affect mitochondrial integrity and function, with Pink1 involved in mitochondrial fusion and Parkin in mitophagy. In Alzheimer's disease, mitochondrial dysfunction is linked to amyloid-beta accumulation and increased mitochondrial fission. In Huntington's disease, mutant huntingtin disrupts mitochondrial dynamics, leading to mitochondrial dysfunction and neurodegeneration. Overall, mitochondrial dynamics are integral to neuronal health, and understanding these processes may lead to new therapeutic strategies for neurodegenerative diseases.