Mitochondrial dysfunction is a common characteristic of all neurodegenerative 
diseases. However, the cause of this dysfunction remains a mystery. Here, we 
discuss the potential role of mitochondrial fission and fusion in the onset and 
progression of neurodegenerative diseases. Specifically, we propose that an 
imbalance in mitochondrial fission and fusion may underlie both familial and 
sporadic neurodegenerative disorders. There is substantial evidence that links 
disruption of the mitochondrial fission and fusion equilibrium, resulting in 
abnormally long or short mitochondria, to neurodegeneration. First, hereditary 
mutations in the mitochondrial fusion GTPases optic atrophy-1 and mitofusin-2 
cause neuropathies in humans. In addition, recent findings report increased 
mitochondrial fission in Parkinson's disease (PD) models and induction of 
mitochondrial fission by two proteins, PTEN-induced kinase 1 and parkin, which 
are mutant in familial forms of PD. Furthermore, mutant huntingtin, the 
disease-causing protein in Huntington's disease, alters mitochondrial morphology 
and dynamics. Rotenone, a pesticide and inducer of PD symptoms, and amyloid-beta 
peptide, which is causally linked to Alzheimer's disease, initiate mitochondrial 
fission. Finally, mitochondrial fission is an early event in ischemic stroke and 
diabetic neuropathies. In sum, a growing body of research suggests that a better 
understanding of mitochondrial fission and fusion and the regulatory factors 
involved may lead to improved treatments and cures for neurodegenerative 
diseases.