More strikingly, the GFAP-TGF-β1 mice (without overexpressing mutant APP) develop an AD-like cerebrovascular pathology, including a reduction in CBF and increase in perivascular Aβ accumulation [58], further supporting the idea that astrocyte TGF-β1 can directly induce an AD-like vascular and amyloid pathology. This evidence concerns the gene TGFB1 and amyloidosis.