Journal
SEMINARS IN IMMUNOPATHOLOGY
Volume 35, Issue 3, Pages 277-292Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s00281-013-0373-9
Keywords
Alzheimer's disease; Amyloid-beta; APP; Protein misfolding; ER stress; UPR
Categories
Funding
- 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
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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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