Supporting this hypothesis, (i) LRP1 is known to contribute to the clearance of beta-amyloid from the brain to the periphery (for review see [44]), (ii) we detected the levels of LRP1 to be significantly increased selectively in the AD OM fibroblast/stromal-like cells, and (iii) we did not observe altered levels of the beta-amyloid influx receptor RAGE in AD OM fibroblast/stromal like cells (for review on the role of LRP1 in beta-amyloid clearance see [44]). The gene discussed is LRP1; the disease is Alzheimer disease.