Journal
CURRENT NEUROLOGY AND NEUROSCIENCE REPORTS
Volume 9, Issue 3, Pages 212-219Publisher
SPRINGER
DOI: 10.1007/s11910-009-0032-7
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Funding
- McKnight Foundation (Brain Disorders Award)
- National Institutes of Health [R01AR054926, R21NS056878]
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR054926] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF MENTAL HEALTH [R01MH080378] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R21NS056878] Funding Source: NIH RePORTER
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Mitochondria are key organelles in eukaryotic cells that not only generate adenosine triphosphate but also perform such critical functions as hosting essential biosynthetic pathways, calcium buffering, and apoptotic signaling. In vivo, mitochondria form dynamic networks that undergo frequent morphologic changes through fission and fusion. In neurons, the imbalance of mitochondrial fission/fusion can influence neuronal physiology, such as synaptic transmission and plasticity, and affect neuronal survival. Core components of the mitochondrial fission/fusion machinery have been identified through genetic studies in model organisms. Mutations in some of these genes in humans have been linked to rare neurodegenerative diseases such as Charcot-Marie-Tooth subtype 2A and autosomal dominant optic atrophy. Recent studies also have implicated aberrant mitochondrial fission/fusion in the pathogenesis of more common neurodegenerative diseases such as Parkinson's disease. These studies establish mitochondrial dynamics as a new paradigm for neurodegenerattve disease research. Compounds that modulate mitochondrial fission/fusion could have therapeutic value in disease intervention.
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