Fig. 5

IPAD in α-DB deficient mice. In wild-type control mice, Aβ was observed diffusely distributed in the parenchyma (e and d) and co-localised with collagen IV in the walls of arterioles (white arrows), capillaries (yellow arrow) and few venules (green arrow). In α-DB deficient mice, the fluorescence due to Aβ appeared more intense in the parenchyma (k and I) but also co-localised with collagen IV in the walls of arterioles (white arrows) and few venules (green arrow). Representative high-power images of an arteriole shows amyloid-β (red) in the wall of the blood vessel, indicated by the white arrow in both wild-type control (e–h) and -DB deficient mice (m–p). Scale bars a–d and I–l = 200 µm, e–h and m-p = 10 µm. There was no difference in vessel density of capillaries or arterioles between wild-type control and α-DB deficient mice, but α-DB deficient mice showed both a significantly lower density of venules (q) and a significantly lower density of Aβ positive arterioles (r). The spread of Aβ in the parenchyma as measured by surface area was similar between wild-type control and α-DB deficient mice (s) but fluorescent intensity was significantly greater in α-DB deficient mice (t). Each box plot represents the range of data from five mice. The scatter plots represent vessel density (q and r), fluorescent area (s) or pixel density (t) from each mouse