Journal
NEUROSCIENTIST
Volume 22, Issue 3, Pages 266-277Publisher
SAGE PUBLICATIONS INC
DOI: 10.1177/1073858415574600
Keywords
complex I; apoptosis; fusion/fission; mtDNA; mitochondria-associated endoplasmic reticulum membranes
Categories
Funding
- Fondo de Investigacion Sanitaria, Instituto de Salud Carlos III (FIS-ISCIII, Spain)
- Ministerio de Ciencia e Innovacion (MICINN, Spain)
- Fundacio Marato de TV3 (Spain)
- Centro de Investigacion Biomedica en Red en Enfermedades Neurodegenerativas (CIBERNED, Instituto de Salud Carlos III, Spain)
- Ramon y Cajal Program from MICINN (Spain)
- Ministerio de educacion, cultura y deporte (FPU, Spain) [FPU13/01339]
- ICREA Funding Source: Custom
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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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