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Biomolecules 2015, 5(4), 2675-2700; doi:10.3390/biom5042675

Αlpha-Synuclein as a Mediator in the Interplay between Aging and Parkinson’s Disease

Brain Mind Institute, Ecole Polytechnique Fédérale de Lausanne (EPFL), Lausanne 1015, Switzerland
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Academic Editor: Stephan N. Witt
Received: 13 August 2015 / Revised: 22 September 2015 / Accepted: 13 October 2015 / Published: 16 October 2015
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Abstract

Accumulation and misfolding of the alpha-synuclein protein are core mechanisms in the pathogenesis of Parkinson’s disease. While the normal function of alpha-synuclein is mainly related to the control of vesicular neurotransmission, its pathogenic effects are linked to various cellular functions, which include mitochondrial activity, as well as proteasome and autophagic degradation of proteins. Remarkably, these functions are also affected when the renewal of macromolecules and organelles becomes impaired during the normal aging process. As aging is considered a major risk factor for Parkinson’s disease, it is critical to explore its molecular and cellular implications in the context of the alpha-synuclein pathology. Here, we discuss similarities and differences between normal brain aging and Parkinson’s disease, with a particular emphasis on the nigral dopaminergic neurons, which appear to be selectively vulnerable to the combined effects of alpha-synuclein and aging. View Full-Text
Keywords: alpha-synuclein; Parkinson’s disease; aging; mitochondria; proteostasis; nigral dopaminergic neurons; metabolism alpha-synuclein; Parkinson’s disease; aging; mitochondria; proteostasis; nigral dopaminergic neurons; metabolism
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Bobela, W.; Aebischer, P.; Schneider, B.L. Αlpha-Synuclein as a Mediator in the Interplay between Aging and Parkinson’s Disease. Biomolecules 2015, 5, 2675-2700.

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