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Neuroscientist. 2016 Jun;22(3):266-77. doi: 10.1177/1073858415574600. Epub 2015 Mar 11.

The Parkinson Disease Mitochondrial Hypothesis: Where Are We at?

Author information

1
Vall d'Hebron Research Institute-CIBERNED, Barcelona, Spain.
2
Vall d'Hebron Research Institute-CIBERNED, Barcelona, Spain Catalan Institution for Research and Advanced Studies (ICREA), Barcelona, Spain Department of Biochemistry and Molecular Biology, Autonomous University of Barcelona, Barcelona, Spain.
3
Vall d'Hebron Research Institute-CIBERNED, Barcelona, Spain celine.perier@vhir.org.

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.

KEYWORDS:

apoptosis; complex I; fusion/fission; mitochondria-associated endoplasmic reticulum membranes; mtDNA

PMID:
25761946
DOI:
10.1177/1073858415574600
[Indexed for MEDLINE]

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