APOA1 and amyloidosis: Specifically, transgenic overexpression of human apoA-I, the major protein component on HDL, from its endogenous promoter in the liver and intestine, reduces neuroinflammation, improves cognitive function and selectively reduces cerebrovascular amyloid in the APP/PS1 model of amyloidosis, whereas deletion of apoA-I, the major protein component of HDL, has the opposite effects [13, 14].