Journal
TRENDS IN BIOCHEMICAL SCIENCES
Volume 40, Issue 4, Pages 200-210Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tibs.2015.02.003
Keywords
mitochondrial dysfunction; Parkinson's disease; mitophagy; oxidative stress; alpha-synuclein
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Funding
- Monument Discovery Award from Parkinson's UK
- Parkinson's UK [G-0801, G-1003]
- Canadian Institutes of Health Research (CIHR)
- National Scholar Award from the Fonds de Recherche du Quebec Sante (FRSQ)
- Parkinson's UK [J-0901] Funding Source: researchfish
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Parkinson's disease (PD) is a progressive neurodegenerative disorder characterised by the preferential loss of dopaminergic neurons in the substantia nigra. Mitochondrial dysfunction is increasingly appreciated as a key determinant of dopaminergic neuronal susceptibility in PD and is a feature of both familial and sporadic disease, as well as in toxin-induced Parkinsonism. Recently, the mechanisms by which PD-associated mitochondrial proteins phosphatase and tensin homolog deleted on chromosome 10 (PTEN)-induced putative kinase 1 (PINK1) and parkin function and induce neurodegeneration have been identified. In addition, increasing evidence implicates other PD-associated proteins such as alpha-synuclein (alpha-syn) and leucine-rich repeat kinase 2 (LRRK2) in mitochondrial dysfunction in genetic cases of PD with the potential for a large functional overlap with sporadic disease. This review highlights how recent advances in understanding familial PD-associated proteins have identified novel mechanisms and therapeutic strategies for addressing mitochondrial dysfunction in PD.
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