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Role of Perivascular Cells and Myocytes in Vascular Amyloidosis
Author(s) -
WISNIEWSKI H. M.,
WEGIEL J.,
VORBRODT A. W.,
MAZURKOLECKA B.,
FRACKOWIAK J.
Publication year - 2000
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2000.tb06344.x
Subject(s) - parenchyma , pathology , pericyte , necrosis , perivascular space , myocyte , amyloidosis , vascular smooth muscle , amyloid (mycology) , chemistry , microglia , biology , endothelial stem cell , inflammation , microbiology and biotechnology , medicine , smooth muscle , endocrinology , immunology , biochemistry , in vitro
A bstract : Amyloidogenic processing of amyloid‐β precursor protein (APP) by cells of the brain is the major pathologic component of Alzheimer's disease. Amyloid‐β (Aβ) is of heterogenous origin. Perivascular cells of monocyte‐macrophage‐microglial cell lineage produce fibrillar Aβ in the wall of capillaries, whereas parenchymal microglial cells produce fibrillar Aβ in the parenchyma of gray matter. Fibrillar Aβ deposition by perivascular cells leads to endothelial cell degeneration and death, obliteration of affected capillaries, and reduction of the length of the vascular network. These changes cause local ischemia with neuronal degeneration and death. Smooth muscle cells are the source of Aβ in the tunica media of parenchymal and leptomeningeal arteries and veins. Fibrillar Aβ in the tunica media of leptomeningeal and parenchymal vessels causes degeneration and necrosis of smooth muscle cells and leads to multiple cortical hemorrhages. Smooth muscle cells isolated from blood vessels with amyloid deposits secrete Aβ and accumulate nonfibrillar Aβ intracellularly. The amyloidogenic processing of APP can be enhanced by apolipoprotein E, reduced by transthyretin, and modulated by several cytokines.