Cellular Proteostasis in Neurodegeneration

被引:0
|
作者
Alberim Kurtishi
Benjamin Rosen
Ketan S. Patil
Guido W. Alves
Simon G. Møller
机构
[1] St. John’s University,Department of Biological Sciences
[2] Stavanger University Hospital,Norwegian Center for Movement Disorders
来源
Molecular Neurobiology | 2019年 / 56卷
关键词
Neurodegeneration; Proteostasis; Aggregation; Chaperone; Autophagy; Ubiquitin; ER; Proteotoxicity; Apoptosis; ROS; Lewy bodies;
D O I
暂无
中图分类号
学科分类号
摘要
The term proteostasis reflects the fine-tuned balance of cellular protein levels, mediated through a vast network of biochemical pathways. This requires the regulated control of protein folding, post-translational modification, and protein degradation. Due to the complex interactions and intersection of proteostasis pathways, exposure to stress conditions may lead to a disruption of the entire network. Incorrect protein folding and/or modifications during protein synthesis results in inactive or toxic proteins, which may overload degradation mechanisms. Further, a disruption of autophagy and the endoplasmic reticulum degradation pathway may result in additional cellular stress which could ultimately lead to cell death. Neurodegenerative diseases such as Parkinson’s disease, Alzheimer’s disease, Huntington’s disease, and Amyotrophic Lateral Sclerosis all share common risk factors such as oxidative stress, aging, environmental stress, and protein dysfunction; all of which alter cellular proteostasis. The differing pathologies observed in neurodegenerative diseases are determined by factors such as location-specific neuronal death, source of protein dysfunction, and the cell’s ability to counter proteotoxicity. In this review, we discuss how the disruption in cellular proteostasis contributes to the onset and progression of neurodegenerative diseases.
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页码:3676 / 3689
页数:13
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