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

Biomolecules

Wojciech Bobela²  Patrick Aebischer²  Bernard Laurent Schneider¹ 

[1] Brain Mind Institute, Ecole Polytechnique Fédérale de Lausanne (EPFL), Lausanne 1015, Switzerland;

关键词: alpha-synuclein;    Parkinson’s disease;    aging;    mitochondria;    proteostasis;    nigral dopaminergic neurons;    metabolism;   

DOI  :  10.3390/biom5042675

来源: mdpi

【 摘 要 】

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.

【 授权许可】

CC BY   
© 2015 by the authors; licensee MDPI, Basel, Switzerland.