Neurobiology of Aging
Volume 33, Issue 3 , Pages 437-456, March 2012

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

  • Rita J. Guerreiro

      Affiliations

    • Laboratory of Neurogenetics, National Institute of Aging, National Institutes of Health, Bethesda, MD, USA
    • Centre for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal
    • Corresponding Author InformationCorresponding author at. Tel.: 301 435 8866; fax: 301 451 7295
  • ,
  • Deborah R. Gustafson

      Affiliations

    • Neuropsychiatric Epidemiology Unit, Sahlgrenska Academy, University of Gothenburg, Sweden
    • Departments of Neurology and Medicine, SUNY-Downstate Medical Center, Brooklyn, NY, USA
  • ,
  • John Hardy

      Affiliations

    • Reta Lila Weston Institute and Departments of Molecular Neuroscience and Neurodegenerative Disease, Institute of Neurology, London, UK

Received 9 September 2009; received in revised form 1 March 2010; accepted 11 March 2010. published online 01 July 2010.

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.

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PII: S0197-4580(10)00220-4

doi:10.1016/j.neurobiolaging.2010.03.025

Neurobiology of Aging
Volume 33, Issue 3 , Pages 437-456, March 2012