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Current Alzheimer Research

Editor-in-Chief

ISSN (Print): 1567-2050
ISSN (Online): 1875-5828

The Role of ER Stress-Induced Apoptosis in Neurodegeneration

Author(s): Ioanna C. Stefani, Daniel Wright, Karen M. Polizzi and Cleo Kontoravdi

Volume 9, Issue 3, 2012

Page: [373 - 387] Pages: 15

DOI: 10.2174/156720512800107618

Price: $65

Abstract

Post-mortem analyses of human brain tissue samples from patients suffering from neurodegenerative disorders have demonstrated dysfunction of the endoplasmic reticulum (ER). A common characteristic of the aforementioned disorders is the intracellular accumulation and aggregation of proteins due to genetic mutations or exogenous factors, leading to the activation of a stress mechanism known as the unfolded protein response (UPR). This mechanism aims to restore cellular homeostasis, however, if prolonged, can trigger pro-apoptotic signals, which are thought to contribute to neuronal cell death. The authors present evidence to support the role of ER stress-induced apoptosis in Alzheimer’s, Parkinson’s and Huntington’s diseases, and further examine the interplay between ER dyshomeostasis and mitochondrial dysfunction, and the function of reactive oxygen species (ROS) and calcium ions (Ca2+) in the intricate relationship between the two organelles. Possible treatments for neurodegenerative diseases that are based on combating ER stress are finally presented.

Keywords: Apoptosis, calcium dyshomeostasis, endoplasmic reticulum stress, neurodegeneration, oxidative stress, reactive oxygen species


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