Here, we are interested in identifying genetic variants specifically associated with a high abundance of amyloid deposits and neurofibrially tangles in the brain, which we refer to as “histopathologically defined AD.”[1] Specifically, we are interested in whether carrying the ApoE ε4 variant, which in the study is considered the “environmental variable”, modifies the effect of SNPs residing in Toll-Like Receptors (TLR) and Receptor for advanced glycation end products (RAGE) on histopathologically defined AD. The gene discussed is AGER; the disease is Alzheimer disease.