期刊
CURRENT OPINION IN CELL BIOLOGY
卷 23, 期 2, 页码 239-252出版社
CURRENT BIOLOGY LTD
DOI: 10.1016/j.ceb.2011.01.003
关键词
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类别
资金
- FONDECYT [1100176]
- FONDAP [15010006]
- Millennium Nucleus [P07-048-F]
- CHDI Foundation Inc
- Genzyme
- Alzheimer's Association [NIRG-10-173294]
- M.J. Fox Foundation for Parkinson's Research
- ICGEB
- ALSA-The Milton Safenowitz Post-Doctoral Fellowship for ALS Research [1829]
- CONICYT [79100007]
- National Institutes of Health [AI32412]
- Mathers Foundation
Several neurodegenerative diseases share common neuropathology, primarily featuring the presence in the brain of abnormal protein inclusions containing specific misfolded proteins. Recent evidence indicates that alteration in organelle function is a common pathological feature of protein misfolding disorders, highlighting perturbations in the homeostasis of the endoplasmic reticulum (ER). Signs of ER stress have been detected in most experimental models of neurological disorders and more recently in brain samples from human patients with neurodegenerative disease. To cope with ER stress, cells activate an integrated signaling response termed the unfolded protein response (UPR), which aims to reestablish homeostasis in part through regulation of genes involved in protein folding, quality control and degradation pathways. Here we discuss the particular mechanisms currently proposed to be involved in the generation of protein folding stress in different neurodegenerative conditions and speculate about possible therapeutic interventions.
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