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Fig. 2 | BMC Neurology

Fig. 2

From: Can brain impermeable BACE1 inhibitors serve as anti-CAA medicine?

Fig. 2

Microscopic images and schematic drawings illustrating a hypothetic model of cerebral amyloid angiopathy. Panels (a-f) show arterioles without (a) and with β-amyloid labeling of increasing intensity. Aβ deposition appears to occur around the tunica intima or endothelial layer (b, c), then emerges and accumulates in the tunica media (TM) (c-f). Perivascular deposition (arrowheads) is seen around vessels with mild to severe Aβ labeling in the vascular wall (c-f). Panels (f-j) are images of β-secretase 1 (BACE1) immunolabeling with h.e. counterstain, showing arterioles without (f) and with immunolabeled elements exhibiting a progressive pattern (g-j). Thus, BACE1 labeling is identifiable at the endothelial layer in (g, h), occurs at the perivascular zone in (h) and presents across the vascular wall and perivascular zone in (i, j). Arrows point to compact plaques. Scale bar = 50 μm in (a) applying to (b-g, i, j), equal to 100 μm for (h). Panel (k) illustrates a hypothetic model for BACE1 elevation in vascular and brain-specific cellular elements in the development of CAA. BACE1 elevation first occurs in endothelial cells (ECs), resulting in Aβ accumulation in the smooth muscle cell (SMC) layer. This causes damage of tight junctions (TJ) and leakage of blood contents into the SMC layer (curved arrows). Aβ and blood infiltration then induce SMC degeneration, triggering aberrant sprouting of the perivascular axonal terminals inherent neuronal Aβ overproduction. This process continues progressively and may end up with a “burnout” stage whereby the ECs, SMCs and dystrophic neurites all degenerate. This figure is adapted with modification from Fig. 7 in [25]

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