APOA1 and amyloidosis: Conversely, apoA-I overexpression from its native promoter reduces CAA and neuroinflammation [20], and delivery of recombinant HDL or apoA-I Milano (an atheroprotective apoA-I genetic variant) into the systemic circulation of mice acutely decreases soluble brain Aβ levels and leads to long-lasting lowering of CAA and neuroinflammation, respectively [13, 14], suggesting the potential for HDL to play a role in removing pre-existing vascular amyloid deposits in vivo.