Elimination of Lrp1 expression in the CA fields and dentate gyrus of the hippocampus had no effect on the severity of amyloid deposition, the rate of Aβ40/42 accumulation, or the architecture of amyloid plaques in the hippocampus in APPswe/PS1dE9 transgenic mice, indicating that expression of Lrp1 protein by neurons in proximity to senile amyloid plaques does not appear to play a major role in modulating the formation of these proximal deposits or in the appearance of the associated neuritic pathology [61]. This evidence concerns the gene LRP1 and amyloidosis.