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      Mitochondrial dysfunction and mitophagy in Parkinson's: from familial to sporadic disease.

      Trends in Biochemical Sciences
      Animals, Humans, Mitochondria, metabolism, pathology, Parkinson Disease, alpha-Synuclein

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          Abstract

          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 α-synuclein (α-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. Copyright © 2015 Elsevier Ltd. All rights reserved.

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          Author and article information

          Journal
          25757399
          10.1016/j.tibs.2015.02.003

          Chemistry
          Animals,Humans,Mitochondria,metabolism,pathology,Parkinson Disease,alpha-Synuclein
          Chemistry
          Animals, Humans, Mitochondria, metabolism, pathology, Parkinson Disease, alpha-Synuclein

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