Non-CAA angiopathies and their possible interactions with cerebral amyloidangiopathy

Citation
Hv. Vinters et Zz. Wang, Non-CAA angiopathies and their possible interactions with cerebral amyloidangiopathy, AMYLOID, 8, 2001, pp. 2-9
Citations number
34
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Medical Research General Topics
Journal title
AMYLOID-JOURNAL OF PROTEIN FOLDING DISORDERS
ISSN journal
1350-6129 → ACNP
Volume
8
Year of publication
2001
Supplement
1
Pages
2 - 9
Database
ISI
SICI code
1350-6129(200107)8:<2:NAATPI>2.0.ZU;2-T
Abstract
Cerebral amyloid angiopathy (CAA) is one of the two most common cerebral ar teriopathies seen in the brains of elderly patients. The other is arteriosc lerosis (AS), historically considered a consequence of chronic hypertension and also described as lipohyalinosis (LH), a clinicopathologic association that is increasingly questioned. These and other less frequently encounter ed degenerations of the cerebral microvasculature (CADASIL, Binswanger subc ortical leukoencephalopathy) share the common feature of degeneration of th e medial smooth muscle layer within arteriolar walls. This can be dramatic in CAA, in the course of which complete replacement of medial smooth muscle by, fibrillar amyloid may occur It is a less prominent feature of CADASIL and BSLE; in the latter condition, medial smooth muscle hyperplasia, possib ly a response to some kind of injury, is a more dramatic finding. In some o f these "angiomyopathies", fibrinoid necrosis of the arterial wall and micr oaneurysm formation may lead to stroke, manifest as cerebral hemorrhage. Wi th CADASIL and BSLE, ischemic brain injury is more common. In the case of C AA upregulation of the A beta -amyloid precursor protein occurs when arteri olar smooth muscle cells in culture are exposed to prolonged hypoxia, espec ially, with reoxygenation. Injury, to arteriolar smooth muscle cells may be one mechanism by which angiomyopathies progress and become symptomatic.