Commentary

Stephen      D. Skaper

doi:10.2174/187152712800672391

Abstract

Parkinson's disease (PD), the most frequent movement disorder, is caused by the progressive loss of the dopamine neurons within the substantia nigra pars compacta and the associated deficiency of the neurotransmitter dopamine in the striatum. Most cases of PD are of a sporadic nature whose cause is unknown, while mutations in several genes have been linked to genetic forms of PD (α-synuclein, Parkin, DJ-1, PINK1, and LRRK2). Epidemiological studies in humans, as well as molecular studies in toxin-induced (e.g. 6-hydroxydopamine (6-OHDA) and rotenone) and genetic animal models of PD show that mitochondrial dysfunction, especially Complex I, is a defect occurring early in the pathogenesis of both sporadic and familial PD. Mitochondrial dynamics (fission, fusion, migration) are important for neurotransmission, synaptic maintenance and neuronal survival.....

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