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Figure 2 | Molecular Medicine

Figure 2

From: Cortical and Leptomeningeal Cerebrovascular Amyloid and White Matter Pathology in Alzheimer’s Disease

Figure 2

Electron micrographs of a normal cortical artery and of arteries destroyed by amyloid deposition in 3 AD cases homozygous for Apo E ε4/ε4. A: An electron micrograph of a small normal cortical artery. The endothelial cells are joined by tight junctions (small arrows) that participate in the blood-brain barrier. Both their nuclei and thin cytoplasm have a normal morphology. These cells are in contact with the subjacent basal lamina (opposing large arrows). The smooth muscle cells (white arrows) have a normal-looking fibrillar cytoplasm, and a typical nucleus is seen on the left margin of the photograph. The thin periarterial space (black arrowheads) contains the extracellular matter of the adventitia and is on its outer margin limited by a single layer of pial cells (8). Magnification 5500×. B and C: Small cortical arteries surrounded by heavy amyloid deposition. The endothelial cells are apparently swollen. The tight junctions have an abnormal morphology (black arrows). The dense amyloid deposits are fused with the basal lamina of the vascular cells. The myocytes have vanished or are reduced to a collection of cellular debris (white arrows) that is enclosed by concentric layers and peripheral wisps of amyloid surrounded by a large amount of tissue debris (open stars). The tunica adventitia, perivascular spaces, and the glia limitans have degenerated as the result of heavy amyloid deposition. Magnification 4300× and magnification 3500×, respectively. D: An abnormal cortical artery with abundant fine wisps of amyloid perpendicular to the main axis of the vessel. The amyloid bundles, interspersed by large amounts of cellular debris, pushed out the glia limitans (open arrows). On the left margin of the micrograph, the amyloid has destroyed the glia limitans invading the surrounding cortical tissue (black stars). All myocytes and the tunica adventitia have been replaced by amyloid fibrils and debris. Magnification 2000×. One may assume from the extensive vascular pathology that the delivery of oxygen and nutrients as well as arterial contractility are largely compromised.

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