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10.1007/s11910-018-0829-3

http://scihub22266oqcxt.onion/10.1007/s11910-018-0829-3
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C5882770!5882770!29616350
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suck abstract from ncbi


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pmid29616350      Curr+Neurol+Neurosci+Rep 2018 ; 18 (5): ä
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  • Mitochondrial Dysfunction in Parkinson?s Disease: New Mechanistic Insights and Therapeutic Perspectives #MMPMID29616350
  • Park JS; Davis RL; Sue CM
  • Curr Neurol Neurosci Rep 2018[]; 18 (5): ä PMID29616350show ga
  • Purpose of Review: Parkinson?s disease (PD) is a complex neurodegenerative disorder, the aetiology of which is still largely unknown. Overwhelming evidence indicates that mitochondrial dysfunction is a central factor in PD pathophysiology. Here we review recent developments around mitochondrial dysfunction in familial and sporadic PD, with a brief overview of emerging therapies targeting mitochondrial dysfunction. Recent Findings: Increasing evidence supports the critical role for mitochondrial dysfunction in the development of sporadic PD, while the involvement of familial PD-related genes in the regulation of mitochondrial biology has been expanded by the discovery of new mitochondria-associated disease loci and the identification of their novel functions. Summary: Recent research has expanded knowledge on the mechanistic details underlying mitochondrial dysfunction in PD, with the discovery of new therapeutic targets providing invaluable insights into the essential role of mitochondria in PD pathogenesis and unique opportunities for drug development.
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