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SCIENTIFIC LITERATURE · MED

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

J Biol Chem · 2012-10-19

DOI: 10.1074/jbc.r112.410530PMID: 23086948

Check source for accessResearch Support, Non-U.S. Gov't; review-article; Review; Research Support, U.S. Gov't, Non-P.H.S.; Journal Article; Research Support, N.I.H., ExtramuralOriginal source ↗

Research overview

The text below is the source article’s original abstract under a verified reuse license. cc by

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 Ca(2+) 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 voltage-dependent channels (channels for which there are brain-penetrant antagonists approved for human use), a neuroprotective strategy to reduce this burden is available.

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