The genetic architecture of Alzheimer's disease: beyond APP, PSENs and APOE

被引:180
作者
Guerreiro, Rita J. [1 ,2 ]
Gustafson, Deborah R. [3 ,4 ,5 ]
Hardy, John [6 ,7 ,8 ]
机构
[1] NIA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA
[2] Univ Coimbra, Ctr Neurosci & Cell Biol, Coimbra, Portugal
[3] Univ Gothenburg, Neuropsychiat Epidemiol Unit, Sahlgrenska Acad, Gothenburg, Sweden
[4] Suny Downstate Med Ctr, Dept Neurol, Brooklyn, NY 11203 USA
[5] Suny Downstate Med Ctr, Dept Med, Brooklyn, NY 11203 USA
[6] Reta Lila Weston Inst, London, England
[7] Inst Neurol, Dept Mol Neurosci, London WC1N 3BG, England
[8] Inst Neurol, Dept Neurodegenerat Dis, London WC1N 3BG, England
基金
美国国家卫生研究院;
关键词
GENOME-WIDE ASSOCIATION; AMYLOID-BETA-PEPTIDE; SINGLE-NUCLEOTIDE POLYMORPHISMS; APOLIPOPROTEIN-E GENOTYPE; TOTAL CHOLESTEROL LEVELS; MEMBRANE-ATTACK COMPLEX; CONVERTING ENZYME GENE; VASCULAR RISK-FACTORS; BODY-MASS INDEX; LINKAGE ANALYSIS;
D O I
10.1016/j.neurobiolaging.2010.03.025
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
Alzheimer's disease (AD) is a complex disorder with a clear genetic component. Three genes have been identified as the cause of early onset familial AD (EOAD). The most common form of the disease, late onset Alzheimer's disease (LOAD), is, however, a sporadic one presenting itself in later stages of life. The genetic component of this late onset form of AD has been the target of a large number of studies, because only one genetic risk factor (APOE4) has been consistently associated with the disease. However, technological advances allow new approaches in the study of complex disorders. In this review, we discuss the new results produced by genome wide association studies, in light of the current knowledge of the complexity of AD genetics. Published by Elsevier Inc.
引用
收藏
页码:437 / 456
页数:20
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