A new study conducted by researchers at the University of Eastern Finland discovered that the APP A673T genetic variant, which protects against Alzheimer’s disease, alters levels of several proteins and peptides linked to amyloid-beta metabolism in human biofluids and cell culture models, including amyloid beta itself. These new data support the idea that even a modest reduction in the beta-amyloidogenic processing of APP may be a feasible strategy for the prevention of Alzheimer’s disease.