期刊
SEMINARS IN IMMUNOPATHOLOGY
卷 35, 期 3, 页码 277-292出版社
SPRINGER HEIDELBERG
DOI: 10.1007/s00281-013-0373-9
关键词
Alzheimer's disease; Amyloid-beta; APP; Protein misfolding; ER stress; UPR
资金
- Alzheimer's Association
- Millennium Institute [P09-015-F]
- Muscular Dystrophy Association
- ALS Therapy Alliance
- FONDECYT [1100176]
- Ring Initiative Act [1109]
- FONDEF [D11I1007]
- Michael J. Fox Foundation for Parkinson Research
- CONICYT
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by synaptic dysfunction and accumulation of amyloid-beta (A beta) peptide, which are responsible for the progressive loss of memory. The mechanisms involved in neuron dysfunction in AD remain poorly understood. Recent evidence implicates the participation of adaptive responses to stress within the endoplasmic reticulum (ER) in the disease process, via a pathway known as the unfolded protein response (UPR). Here, we review the findings suggesting a functional role of ER stress in the etiology of AD. Possible therapeutic strategies to mitigate ER stress in the context of AD are discussed.
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