The genetic architecture of Alzheimer's disease: beyond APP, PSENs and APOE.
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.
Guerreiro
Rita J
RJ
Laboratory of Neurogenetics, National Institute of Aging, National Institutes of Health, Bethesda, MD, USA. portalegrer@nia.nih.gov
Gustafson
Deborah R
DR
Hardy
John
J
D000544:Alzheimer Disease / Q000235:genetics* / Q000378:metabolism / Q000473:pathology*; D016564:Amyloid beta-Protein Precursor / Q000096:biosynthesis / Q000737:chemistry / Q000235:genetics; D000818:Animals; D001057:Apolipoproteins E / Q000096:biosynthesis / Q000737:chemistry / Q000235:genetics*; D006801:Humans; D053764:Presenilin-1 / Q000096:biosynthesis / Q000737:chemistry / Q000235:genetics*; D053766:Presenilin-2 / Q000096:biosynthesis / Q000737:chemistry / Q000235:genetics
D016564:Amyloid beta-Protein Precursor; D001057:Apolipoproteins E; C508853:PSEN1 protein, human; C508861:PSEN2 protein, human; D053764:Presenilin-1; D053766:Presenilin-2