| Literature DB >> 26993573 |
Paula Garcia-Huerta1, Paulina Troncoso-Escudero1, Carolina Jerez2, Claudio Hetz3, Rene L Vidal4.
Abstract
One of the salient features of most neurodegenerative diseases is the aggregation of specific proteins in the brain. This proteostasis imbalance is proposed as a key event triggering the neurodegenerative cascade. The unfolded protein response (UPR) and autophagy pathways are emerging as critical processes implicated in handling disease-related misfolded proteins. However, in some conditions, perturbations in the buffering capacity of the proteostasis network may be part of the etiology of the disease. Thus, pharmacological or gene therapy strategies to enhance autophagy or UPR responses are becoming an attractive target for disease intervention. Here, we discuss current evidence depicting the complex involvement of autophagy and ER stress in brain diseases. Novel pathways to modulate protein misfolding are discussed including the relation between aging and growth factor signaling. This article is part of a Special Issue entitled SI:Autophagy.Entities:
Keywords: Autophagy; ER stress, aggregation, neurodegenerative disease; IGFs; UPR
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Year: 2016 PMID: 26993573 DOI: 10.1016/j.brainres.2016.02.052
Source DB: PubMed Journal: Brain Res ISSN: 0006-8993 Impact factor: 3.252