volume 24, issue 3, P587-597 2011
DOI: 10.3233/jad-2011-101914
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Olivia Belbin, Kristelle Brown, Hui Shi, Christopher Medway, Richard Abraham, Peter Passmore, David Mann, A. David Smith, Clive Holmes, Bernadette McGuinness, David Craig, Donald Warden, Reinhard Heun, Heike Kölsch et al.

Abstract: A key pathological feature of late-onset Alzheimer’s disease (LOAD) is the abnormal extracellular accumulation of the amyloid beta (Aβ) peptide. Thus altered Aβ degradation could be a major contributor to the development of LOAD. Variants in the gene encoding the Aβ-degrading enzyme, angiotensin-1 converting enzyme (ACE) therefore represent plausible candidates for association with LOAD pathology and risk. Following Alzgene meta-analyses of all published case-control studies, the ACE variants rs4291 and rs180…

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