MIHAELA TEMELIE*, DIANA SAVU*#, NICOLETA MOISOI**, MARIA LUIZA FLONTA***
*Department of Life and Environmental Physics, ”Horia Hulubei” National Institute of Physics and Nuclear Engineering, 30 Reactorului St., Măgurele, Bucharest, Romania
**Cell Physiology and Pharmacology Department, University of Leicester, Maurice Shock Building, University Road, Leicester LE1 9HN, United Kingdom
***Department of Anatomy, Animal Physiology and Biophysics, Faculty of Biology, University of Bucharest, 91–95, Splaiul Independenței, Bucharest, Romania
Parkinson’s disease (PD) is the second most common neurodegenerative condition associated with aging. The disease advances over many years and presents progressive cognitive and motor function disturbances, which can lead to incapacity to perform independently daily activities. Environmental factors, aging and genetic susceptibility are recognized factors that contribute to the complex etiology of Parkinson’s disease. Studying genetic models of PD supports the quest to understand causes and mechanisms of neurodegeneration in PD and points toward novel pharmaceutical approaches to tackle the disease progression. Loss-of-function mutations in the mitochondrial protein kinase PINK1 are causative in early onset autosomal recessive Parkinson’s disease. PINK1 is involved in multiple cellular functions including mitochondrial quality control, calcium homeostasis, cell death and survival mechanisms. Here we review key roles of PINK1 in mitochondrial and nonmitochondrial function and emphasize its implication in the etiopathogenesis of PD in comparison to other diseases.
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