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 rs1800… Show more
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