Memory loss in Alzheimer's disease: are the alterations in the UPR network involved in the cognitive impairment?

Claudia Duran-Aniotz,Gabriela Martínez,Claudio Hetz

doi:10.3389/fnagi.2014.00008

Abstract

Memory loss in Alzheimer's disease: are the alterations in the UPR network involved in the cognitive impairment?

Highlights

Alzheimer’s disease (AD) is a progressive and devastating age-related neurodegenerative disorder, involving memory loss and the extracellular deposition in the brain of misfolded and aggregated amyloid beta (Aβ) peptide (Holtzman et al, 2011)
Interesting novel concepts are emerging where endoplasmic reticulum (ER) stress may operates upstream of the generation of Aβ as part of the etiology of the disease (Yoon et al, 2012). Could these findings provide insights about new points for disease intervention? Many recent studies have developed small molecules and gene therapy strategies to alleviate ER stress in vivo, which offers interesting future applications for the development of clinical trials in AD and other diseases (Hetz et al, 2013)
Under diverse stress conditions, including ER stress, inhibition of protein synthesis operates as a survival pathway that is mediated by the phosphorylation of eukaryotic translation initiator factor 2α, referred to as the “integrated stress response.”

Summary

Introduction

Alzheimer’s disease (AD) is a progressive and devastating age-related neurodegenerative disorder, involving memory loss and the extracellular deposition in the brain of misfolded and aggregated amyloid beta (Aβ) peptide (Holtzman et al, 2011). Aβ oligomers are known to induce neuronal loss and dysfunction (Mucke and Selkoe, 2012) and impair synaptic plasticity and memory in animal models of AD (Cleary et al, 2005; Shankar et al, 2008).

Results

Conclusion