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The unfolded protein response in Alzheimer's disease
被引:92
|作者:
Hugo Cornejo, Victor
[1
,2
]
Hetz, Claudio
[1
,2
,3
,4
,5
]
机构:
[1] Univ Chile, Fac Med, Biomed Neurosci Inst, Santiago 7, Chile
[2] Univ Chile, Inst Biomed Sci, Ctr Mol Studies Cell, Santiago, Chile
[3] Neurounion Biomed Fdn, Santiago, Chile
[4] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA
[5] Univ Chile, Cellular & Mol Biol Program, Inst Biomed Sci, Santiago 1027, Chile
关键词:
Alzheimer's disease;
Amyloid-beta;
APP;
Protein misfolding;
ER stress;
UPR;
ENDOPLASMIC-RETICULUM STRESS;
AMYLOID PRECURSOR PROTEIN;
INDUCED NEURONAL DEATH;
A-BETA;
ER STRESS;
GAMMA-SECRETASE;
CELL-DEATH;
SYNAPTIC PLASTICITY;
TAU-HYPERPHOSPHORYLATION;
PROMOTER POLYMORPHISM;
D O I:
10.1007/s00281-013-0373-9
中图分类号:
R392 [医学免疫学];
Q939.91 [免疫学];
学科分类号:
100102 ;
摘要:
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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页码:277 / 292
页数:16
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