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Brain Pathol. 2006 Jan;16(1):60-70.

The role of cystatin C in cerebral amyloid angiopathy and stroke: cell biology and animal models.

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1
Department of Psychiatry, New York University School of Medicine, and Nathan Kline Institute, Orangeburg 10962, USA. elevy@nki.rfmh.org

Abstract

A variant of the cysteine protease inhibitor, cystatin C, forms amyloid deposited in the cerebral vasculature of patients with hereditary cerebral hemorrhage with amyloidosis, Icelandic type (HCHWA-I), leading to cerebral hemorrhages early in life. However, cystatin C is also implicated in neuronal degenerative diseases in which it does not form the amyloid protein, such as Alzheimer disease (AD). Accumulating data suggest involvement of cystatin C in the pathogenic processes leading to amyloid deposition in cerebral vasculature and most significantly to cerebral hemorrhage in patients with cerebral amyloid angiopathy (CAA). This review focuses on cell culture and animal models used to study the role of cystatin C in these processes.

PMID:
16612983
[Indexed for MEDLINE]
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