CADASIL Artery vs Normal Artery

Source: J Neuropathol Exp Neurol  Volume 72, Number 5, May 2013 Ultrastructural Localization of Brain N3ECD in CADASIL

(Click on the image below to go directly to the source article. p. 429 of the paper has a larger and clearer image of the diagram below)

FIGURE 9. Hypothetical scheme showing pathogenetic mechanisms in CADASIL. In normal (control) individuals, tight junctions (arrowheads) between endothelial cells (ECs) sitting on the basal lamina (BL) form the blood-brain barrier (BBB) that protects the brain from cytotoxic substances. Solutes in the ISF drain out of the brain through perivascular drainage pathways driven by vascular pulsation. In CADASIL, there are several changes to the surface between blood and brain parenchyma or CSF at the artery, arteriole, and capillary levels. Most prominently, the arterial wall disintegrates, specifically by VSMC degeneration, EC damage, and enhancement of GOM deposition (black amorphous blobs). These changes may collectively breach the BBB (triangles and squares) and cause injury to perivascular cells (P). The degeneration of VSMC likely reduces vascular tone such that the perivascular drainage of ISF with GOM and other proteins is impeded; this contributes to enlargement of the perivascular space (PVS) and activation of an inflammatory response by macrophages or phagocytic cells (Ph).

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