The Parkinson Disease Mitochondrial Hypothesis: Where Are We at?

The Neuroscientist : a Review Journal Bringing Neurobiology, Neurology and Psychiatry
Sandra Franco-IborraCeline Perier

Abstract

Parkinson's disease is a common, adult-onset neurodegenerative disorder whose pathogenesis is still under intense investigation. Substantial evidence from postmortem human brain tissue, genetic- and toxin-induced animal and cellular models indicates that mitochondrial dysfunction plays a central role in the pathophysiology of the disease. This review discusses our current understanding of Parkinson's disease-related mitochondrial dysfunction, including bioenergetic defects, mitochondrial DNA alterations, altered mitochondrial dynamics, activation of mitochondrial-dependent programmed cell death, and perturbations in mitochondrial tethering to the endoplasmic reticulum. Whether a primary or secondary event, mitochondrial dysfunction holds promise as a potential therapeutic target to halt the progression of neurodegeneration in Parkinson's disease.

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Methods Mentioned

BETA
transgenic
biopsy
nuclear translocation
electron microscopy

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