To this extent our confirmation of increased Trem2+ area around vessels and Trem2 expression in both PVM subsets provides a plausible explanation for increased ARIA in AD patients and establishes a significant connection between Aβ immunotherapy, vascular damage, compromised BBB integrity, and the recruitment of peripheral and vascular resident immune cells to vascular amyloid deposits; therefore, caution should be exercised when considering the combination of amyloid and TREM2 immunotherapies. This evidence concerns the gene TREM2 and amyloidosis.