Interplay of endoplasmic reticulum stress and autophagy in neurodegenerative disorders

The common underlying feature of most neurodegenerative diseases such as Alzheimer disease (AD), prion diseases, Parkinson disease (PD), and amyotrophic lateral sclerosis (ALS) involves accumulation of misfolded proteins leading to initiation of endoplasmic reticulum (ER) stress and stimulation of t...

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Bibliographic Details
Published in:Autophagy 2016-01, Vol.12 (2), p.225-244
Main Authors: Cai, Yu, Arikkath, Jyothi, Yang, Lu, Guo, Ming-Lei, Periyasamy, Palsamy, Buch, Shilpa
Format: Article
Language:English
Subjects:
alzheimer disease
amyotrophic lateral sclerosis and HIV-associated neurocognitive disorders
Animals
Autophagy
Endoplasmic Reticulum Stress
ER stress
Humans
Models, Biological
Neurodegenerative Diseases - pathology
neurodegenerative disorders
Parkinson disease
prion diseases
Review
Unfolded Protein Response
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Summary:The common underlying feature of most neurodegenerative diseases such as Alzheimer disease (AD), prion diseases, Parkinson disease (PD), and amyotrophic lateral sclerosis (ALS) involves accumulation of misfolded proteins leading to initiation of endoplasmic reticulum (ER) stress and stimulation of the unfolded protein response (UPR). Additionally, ER stress more recently has been implicated in the pathogenesis of HIV-associated neurocognitive disorders (HAND). Autophagy plays an essential role in the clearance of aggregated toxic proteins and degradation of the damaged organelles. There is evidence that autophagy ameliorates ER stress by eliminating accumulated misfolded proteins. Both abnormal UPR and impaired autophagy have been implicated as a causative mechanism in the development of various neurodegenerative diseases. This review highlights recent advances in the field on the role of ER stress and autophagy in AD, prion diseases, PD, ALS and HAND with the involvement of key signaling pathways in these processes and implications for future development of therapeutic strategies.
ISSN:1554-8627
1554-8635
DOI:10.1080/15548627.2015.1121360