The intersection between growth factors, autophagy and ER stress: A new target to treat neurodegenerative diseases?
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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.
This work was funded by FONDECYT 1150608 (R.V.) and FONDECYT 3150097 (P.C.), Millennium Institute No. P09-015-F, and FONDAP 15150012 (R.V. and C.H.). We also thank the Frick Foundation, ALS Therapy Alliance 2014-F-059, Muscular Dystrophy Association 382453, CONICYT-USA2013-0003, Michael J Fox Foundation for Parkinson's Research, COPEC-UC Foundation, Ecos-Conicyt C13502and FONDECYT no. 1140549, Office of Naval Research-Global (ONR-G) N62909-16-1-2003 and CDMRP Amyotrophic Lateral Sclerosis Research Program (ALSRP) Therapeutic Idea Award AL150111 (C.H.).
Artículo de publicación ISI
Quote ItemBrain Research 1649 (2016) 173–180
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