Calcium homeostasis, selective vulnerability and Parkinson's disease

C. Savio Chan*, Tracy S. Gertler, D. James Surmeier

*Corresponding author for this work

Research output: Contribution to journalReview article

154 Scopus citations

Abstract

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 substantia 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.

Original languageEnglish (US)
Pages (from-to)249-256
Number of pages8
JournalTrends in Neurosciences
Volume32
Issue number5
DOIs
StatePublished - May 2009

ASJC Scopus subject areas

  • Neuroscience(all)

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