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- W2034939939 abstract "Parkinson's disease (PD) is the second most common neurodegenerative disease in developed countries. The core motor symptoms are attributable to the degeneration of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNc). Why these neurons succumb in PD is not clear. One potential clue has come from the observation that the engagement of l-type Ca2+ channels during autonomous pacemaking elevates the sensitivity of SNc DA neurons to mitochondrial toxins used to create animal models of PD, suggesting that Ca2+ entry is a factor in their selective vulnerability. Recent work has shown that this Ca2+ entry also elevates mitochondrial oxidant stress and that this stress is exacerbated by deletion of DJ-1, a gene associated with an early onset, recessive form of PD. Epidemiological data also support a linkage between l-type Ca2+ channels and the risk of developing PD. This review examines the hypothesis that the primary factor driving neurodegenerative changes in PD is the metabolic stress created by Ca2+ entry, particularly in the face of genetic or environmental factors that compromise oxidative defenses or proteostatic competence. This article is part of a Special Issue entitled: Function and Dysfunction of the Basal Ganglia." @default.
- W2034939939 created "2016-06-24" @default.
- W2034939939 creator A5033742239 @default.
- W2034939939 creator A5078157864 @default.
- W2034939939 creator A5079470044 @default.
- W2034939939 creator A5081897750 @default.
- W2034939939 date "2011-12-01" @default.
- W2034939939 modified "2023-10-18" @default.
- W2034939939 title "The role of calcium and mitochondrial oxidant stress in the loss of substantia nigra pars compacta dopaminergic neurons in Parkinson's disease" @default.
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