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

Abstract 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...

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Bibliographic Details
Published in:Neurobiology of aging 2012-03, Vol.33 (3), p.437-456
Main Authors: Guerreiro, Rita J, Gustafson, Deborah R, Hardy, John
Format: Article
Language:English
Subjects:
Alzheimer Disease - genetics
Alzheimer Disease - metabolism
Alzheimer Disease - pathology
Amyloid beta-Protein Precursor - biosynthesis
Amyloid beta-Protein Precursor - chemistry
Amyloid beta-Protein Precursor - genetics
Animals
Apolipoproteins E - biosynthesis
Apolipoproteins E - chemistry
Apolipoproteins E - genetics
Humans
Internal Medicine
Neurology
Presenilin-1 - biosynthesis
Presenilin-1 - chemistry
Presenilin-1 - genetics
Presenilin-2 - biosynthesis
Presenilin-2 - chemistry
Presenilin-2 - genetics
Psychiatry
Psykiatri
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Summary:Abstract 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.
ISSN:0197-4580
1558-1497
1558-1497
DOI:10.1016/j.neurobiolaging.2010.03.025