Alpha-Synuclein Toxicity on Protein Quality Control, Mitochondria and Endoplasmic Reticulum
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...
Saved in:
Published in: | Neurochemical research Vol. 43; no. 12; pp. 2212 - 2223 |
---|---|
Main Authors: | , , |
Format: | Journal Article |
Language: | English |
Published: |
New York
Springer US
01-12-2018
Springer Nature B.V |
Subjects: | |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | 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. |
---|---|
ISSN: | 0364-3190 1573-6903 |
DOI: | 10.1007/s11064-018-2673-x |