Transcriptional regulation and its misregulation in Alzheimer's disease

被引：48
作者：
Chen, Xiao-Fen [1 ]
Zhang, Yun-wu [1 ]
Xu, Huaxi [1 ]
Bu, Guojun [1 ]
机构：
[1] Xiamen Univ, Coll Med, Inst Neurosci, Fujian Prov Key Lab Neurodegenerat Dis & Aging Re, Xiamen 361102, Fujian, Peoples R China
来源：
MOLECULAR BRAIN | 2013年 / 6卷
基金：
中国国家自然科学基金;
关键词：
Alzheimer's disease; Transcription factors; Transcriptional regulatory element; Polymorphism; Amyloid-beta; AMYLOID PRECURSOR-PROTEIN; APOLIPOPROTEIN-E GENE; HUMAN PRESENILIN-1 GENE; E APOE LEVELS; BETA-SECRETASE ENZYME; B/REL BINDING-SITE; LIVER-X-RECEPTOR; FACTOR-KAPPA-B; A-BETA; BACE1; EXPRESSION;
D O I：
10.1186/1756-6606-6-44
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
Alzheimer's disease (AD) is a devastating neurodegenerative disorder characterized by loss of memory and cognitive function. A key neuropathological event in AD is the accumulation of amyloid-beta (A beta) peptide. The production and clearance of A beta in the brain are regulated by a large group of genes. The expression levels of these genes must be fine-tuned in the brain to keep A beta at a balanced amount under physiological condition. Misregulation of AD genes has been found to either increase AD risk or accelerate the disease progression. In recent years, important progress has been made in uncovering the regulatory elements and transcriptional factors that guide the expression of these genes. In this review, we describe the mechanisms of transcriptional regulation for the known AD genes and the misregualtion that leads to AD susceptibility.
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页数：9
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