LRP1 and Alzheimer disease: In conclusion, the presented data clearly indicate that in an ischemic model of Alzheimer’s disease, as demonstrated for the first time in our study, reduced RAGE gene expression 30 days post-ischemia likely contributes to the reduction, delay and/or transient inhibition of amyloid accumulation in CA3, and that this effect is maintained and enhanced by a parallel natural increase in LRP1 gene expression.