Calcium, bioenergetics, and neuronal vulnerability in Parkinson's disease

D. James Surmeier*, P. T. Schumacker

*Corresponding author for this work

Research output: Contribution to journalReview article

108 Scopus citations

Abstract

The most distinguishing feature of neurons is their capacity for regenerative electrical activity. This activity imposes a significant mitochondrial burden, especially in neurons that are autonomously active, have broad action potentials, and exhibit prominent Ca2+ entry. Many of the genetic mutations and toxins associated with Parkinson's disease compromise mitochondrial function, providing a mechanistic explanation for the pattern of neuronal pathology in this disease. Because much of the neuronal mitochondrial burden can be traced to L-type voltagedependent channels (channels for which there are brain-penetrantantagonists approved for human use), a neuroprotective strategy to reduce this burden is available.

Original languageEnglish (US)
Pages (from-to)10736-10741
Number of pages6
JournalJournal of Biological Chemistry
Volume288
Issue number15
DOIs
StatePublished - Apr 12 2013

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ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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