Journal
NEUROBIOLOGY OF AGING
Volume 33, Issue 3, Pages 437-456Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2010.03.025
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Funding
- National Institute on Aging, National Institutes of Health, Department of Health and Human Services [Z01 AG000950-06]
- Fundacao para a Ciencia e Tecnologia, Portugal [SFRH/BD/27, 442/2006]
- Swedish MFR
- MRC
- MRC [G0701075, MC_G1000735] Funding Source: UKRI
- Alzheimers Research UK [ART-PPG2011A-14] Funding Source: researchfish
- Medical Research Council [MC_G1000735, G0701075] Funding Source: researchfish
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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.
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