Alpha-Synuclein Toxicity on Protein Quality Control, Mitochondria and Endoplasmic Reticulum.

Alpha-Synuclein Toxicity on Protein Quality Control, Mitochondria and Endoplasmic Reticulum.
Neurochem Res. 2018 Oct 28;:
Authors: Melo TQ, Copray SJCVM, Ferrari MFR
Abstract
Parkinson's disease (PD) is characterized by the presence of insoluble protein clusters containing α-synuclein. Impairment of mitochondria, endoplasmic reticulum, autophagy and intracellular trafficking proper function has been suggested to be caused by α-synuclein toxicity, which is also associated with the higher levels of ROS found in the aged brain and in PD. Oxidative stress leads to protein oligomerization and aggregation that impair autophagy and mitochondrial dynamics leading to a vicious cycle of organelles damage and neurodegeneration. In this review we focused on the role of α-synuclein dysfunction as a cellular stressor that impairs mitochondria, endoplasmic reticulum, autophagy and cellular dynamics culminating with dopaminergic depletion and the pathogenesis of PD.
PMID: 30370500 [PubMed - as supplied by publisher]

Source: Neurochemical Research - October 28, 2018 Category: Neuroscience Authors: Melo TQ, Copray SJCVM, Ferrari MFR Tags: Neurochem Res Source Type: research