Received June 12, 2009; Revised June 12, 2009; Accepted July 16, 2009 | Hsiuchen Chen and David C. Chan*
The article reviews the role of mitochondrial dynamics—fusion, fission, movement, and mitophagy—in neurodegenerative diseases. Mitochondria are dynamic organelles that undergo repeated cycles of fusion and fission, are actively recruited to subcellular sites, and are maintained through mitophagy. Defects in these processes are associated with various neurodegenerative diseases, including Charcot-Marie-Tooth type 2A, dominant optic atrophy, Parkinson’s disease, Alzheimer’s disease, and Huntington’s disease. The article discusses how mitochondrial dynamics is altered in these diseases and the reciprocal interactions between fusion, fission, transport, and mitophagy. Recent findings suggest that manipulating mitochondrial dynamics can partially rescue disease phenotypes, highlighting the potential for therapeutic interventions.The article reviews the role of mitochondrial dynamics—fusion, fission, movement, and mitophagy—in neurodegenerative diseases. Mitochondria are dynamic organelles that undergo repeated cycles of fusion and fission, are actively recruited to subcellular sites, and are maintained through mitophagy. Defects in these processes are associated with various neurodegenerative diseases, including Charcot-Marie-Tooth type 2A, dominant optic atrophy, Parkinson’s disease, Alzheimer’s disease, and Huntington’s disease. The article discusses how mitochondrial dynamics is altered in these diseases and the reciprocal interactions between fusion, fission, transport, and mitophagy. Recent findings suggest that manipulating mitochondrial dynamics can partially rescue disease phenotypes, highlighting the potential for therapeutic interventions.