Publication: Cerebrovascular amyloidosis: Experimental analysis in vitro and in vivo
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Date
1999
Authors
Walker, L.C. ; Durham, R.A.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
With advancing age, the likelihood of Bamyloid
deposition in the cerebral vasculature increases,
particularly in individuals with Alzheimer's disease. The
B-amyloid typically accumulates in the basal lamina of
the arteriolar tunica media, and frequently extends into
the adjacent neuropil. Cerebrovascular B-amyloid
increases the risk of hemorrhagic stroke, and may also
play a role in the pathogenesis of AD. Genetic variations
have been identified that are causative or risk factors for
cerebrovascular B-amyloid, including particular
mutations in the genes for 0-amyloid precursor protein,
presenilins 1 and 2, and possibly cystatin C, as well as
polymorphisms in apolipoprotein E. Cerebrovascular
amyloidosis is now being studied in a variety of in vitro
and in vivo models, including cultured vascular smooth
muscle cells, transgenic mice, and aged animals such as
nonhuman primates. Methods for delivering agents
selectively to vascular amyloid in living subjects are
now being developed, and these techniques are paving
the way to the development of diagnostic tools and
therapies for cerebrovascular amyloidosis.
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