Calcium, Bioenergetics, and Neuronal Vulnerability in Parkinson’s Disease

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

Footnotes

  • * This work was supported, in whole or in part, by National Institutes of Health Grants NS047085, RR025355, and HL35440. This work was also supported by grants from the Hartman Foundation and the United States Army Medical Research and Materiel Command. This article is part of the Thematic Minireview Series on Calcium Function and Disease.

Author: connie dello buono

Health educator, author and enterpreneur motherhealth@gmail.com or conniedbuono@gmail.com ; cell 408-854-1883 Helping families in the bay area by providing compassionate and live-in caregivers for homebound bay area seniors. Blogs at www.clubalthea.com Developing a new site, www.avatarcare.net , for early cancer detection using genetics tests, telemedicine with electronic appointment scheduling with doctors, video chat with doctors, matching care providers with health consumers and a health concierge for all to reduce chronic care cost, find cancer cure and coordinate health care using predictive medicine and participatory.

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