Further, a recent study using animal models of AD, including the lipopolysaccharide (LPS) model of induced inflammation, PS2-APP and human tau expressing transgenic mice lines, APOE knockout and APOE4 knock-in mice showed no evidence of BBB permeability compared to both wild type and a positive multiple sclerosis model control using multiple assays, including Rb-86 radiotracer experiments [36], questioning the long-held belief that BBB disruption is characteristic of AD. The gene discussed is APP; the disease is Alzheimer disease.