Journal
TRENDS IN NEUROSCIENCES
Volume 32, Issue 5, Pages 249-256Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tins.2009.01.006
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Funding
- US Army Medical Research and Material Command and National Institutes of Health [NS047085]
- NATIONAL INSTITUTE OF MENTAL HEALTH [P50MH090963] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [P50NS047085, P30NS054850] Funding Source: NIH RePORTER
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Parkinson's disease (PD) is a common neurodegenerative disorder of which the core motor symptoms are attributable to the degeneration of dopamine (DA) neurons in the substantial nigra pars compacta (SNc). Recent work has revealed that the engagement of L-type Ca2+ channels during autonomous pacemaking renders SNc DA neurons susceptible to mitochondrial toxins used to create animal models of PD, indicating that homeostatic Ca2+ stress could be a determinant of their selective vulnerability. This view is buttressed by the central role of mitochondria and the endoplasmic reticulum (linchpins of current theories about the origins of PD) in Ca2+ homeostasis. Here, we summarize this evidence and suggest the dual roles had by these organelles could compromise their function, leading to accelerated aging of SNc DA neurons, particularly in the face of genetic or environmental stress. We conclude with a discussion of potential therapeutic strategies for slowing the progression of PD.
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