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    • Keywords


      mitochondria; Parkinson’s disease; α-synuclein; ageing; neurodegene

    • Abstract


      Protein aggregation is a hallmark of many neurodegenerative diseases. In Parkinson’s disease protein misfolding of α-synuclein involves conformational changes in the protein structure that often results in self-association and aggregation leading to accumulation of α-synuclein in neuronal cells. The underlying mechanisms by which aggregations can lead to impaired cellular functions are often not understood. Meanwhile, there is growing evidence that links mitochondrial dysfunction to Parkinson’s disease. As both mitochondria and protein aggregation of α-synuclein have been shown to play a major role in Parkinson’s disease, it seems likely that a converging mechanism exists that links the two pathways.

    • Author Affiliations



      1. Department of Cell and Developmental Biology, Hebrew University of Jerusalem, Givat Ram, Jerusalem, Israel
      2. Department of Experimental Neurodegeneration, University Medical Center Gottingen, Waldweg 33, Göttingen, Germany
    • Dates

  • Journal of Genetics | News

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      Posted on July 25, 2019

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