Journal
TRENDS IN NEUROSCIENCES
Volume 37, Issue 6, Pages 315-324Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tins.2014.03.004
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Funding
- NIH/NINDS [NS38377]
- Cure Parkinson's Trust
- JPB Foundation
- Adrienne Helis Malvin Medical Research Foundation
- Johns Hopkins Hospital and the Johns Hopkins University School of Medicine and the Foundation's Parkinson's Disease Program
- Canadian Institutes of Health Research Doctoral Foreign Study Award
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Parkinson's disease (PD) is a progressive neurodegenerative disease that causes a debilitating movement disorder. Although most cases of PD appear to be sporadic, rare Mendelian forms have provided tremendous insight into disease pathogenesis. Accumulating evidence suggests that impaired mitochondria underpin PD pathology. In support of this theory, data from multiple PD models have linked Phosphatase and tensin homolog (PTEN)-induced putative kinase 1 (PINK1) and parkin, two recessive PD genes, in a common pathway impacting mitochondrial health, prompting a flurry of research to identify their mitochondrial targets. Recent work has focused on the role of PINK1 and parkin in mediating mitochondria! autophagy (mitophagy); however, emerging evidence casts parkin and PINK1 as key players in multiple domains of mitochondrial health and quality control.
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