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

作者：Rita Guerreiro, Deborah Gustafson, John Hardy · 发表于：Neurobiology of Aging · 年份：2010 · DOI：10.1016/j.neurobiolaging.2010.03.025 · 被引用次数：282 · 研究领域：Alzheimer's disease research and treatments、Bioinformatics and Genomic Networks、Genetic Associations and Epidemiology

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.