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Cerebral amyloid angiopathy: A microvascular link between parenchymal and vascular dementia?

Cerebral amyloid angiopathy: A microvascular link between parenchymal and vascular dementia? Why should cerebral amyloid (congophilic) angiopathy (CAA) be of interest to neuroscientists? This peculiar cerebral microvascular lesion is one in which arteriolar media, including its smooth muscle cell (SMC) component, is gradually replaced by fibrillar amyloid ( Fig ). 1 The end result of this process is the presence, within cerebral cortex, of markedly weakened arterial walls, which frequently give rise to (lobar) cerebral hemorrhages. 2 , 3 Less often, severe CAA is associated with ischemic brain lesions and granulomatous angiitis. 4 , 5 That CAA is most common and severe in patients with Alzheimer disease (AD) has been well documented in many studies. 6 In this issue of the Annals , Grabowski and colleagues present clinicopathologic details of an Iowa family with autosomal dominant inheritance of a phenotype characterized by progressive aphasic dementia; in one patient who came to necropsy, there was evidence for severe CAA. 7 Of interest is that the clinical and neuropathologic syndrome is linked to a mutation (causing a substitution of asparagine for aspartic acid) at codon 694 of the gene that encodes the amyloid precursor protein (APP), from which Aβ is cleaved. 1 (A) A relatively normal arteriole in a nondemented patient. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annals of Neurology Wiley

Cerebral amyloid angiopathy: A microvascular link between parenchymal and vascular dementia?

Vinters, Harry V.
Annals of Neurology , Volume 49 (6) – Jun 1, 2001
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References (65)

Publisher
Wiley
Copyright
Copyright © 2001 Wiley‐Liss, Inc.
ISSN
0364-5134
eISSN
1531-8249
DOI
10.1002/ana.1055
Publisher site
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Abstract

Why should cerebral amyloid (congophilic) angiopathy (CAA) be of interest to neuroscientists? This peculiar cerebral microvascular lesion is one in which arteriolar media, including its smooth muscle cell (SMC) component, is gradually replaced by fibrillar amyloid ( Fig ). 1 The end result of this process is the presence, within cerebral cortex, of markedly weakened arterial walls, which frequently give rise to (lobar) cerebral hemorrhages. 2 , 3 Less often, severe CAA is associated with ischemic brain lesions and granulomatous angiitis. 4 , 5 That CAA is most common and severe in patients with Alzheimer disease (AD) has been well documented in many studies. 6 In this issue of the Annals , Grabowski and colleagues present clinicopathologic details of an Iowa family with autosomal dominant inheritance of a phenotype characterized by progressive aphasic dementia; in one patient who came to necropsy, there was evidence for severe CAA. 7 Of interest is that the clinical and neuropathologic syndrome is linked to a mutation (causing a substitution of asparagine for aspartic acid) at codon 694 of the gene that encodes the amyloid precursor protein (APP), from which Aβ is cleaved. 1 (A) A relatively normal arteriole in a nondemented patient.

Journal

Annals of Neurology – Wiley

Published: Jun 1, 2001

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