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Co‐localization of β/A4 and cystatin C in cortical blood vessels in Dutch, but not in Icelandic hereditary cerebral hemorrhage with amyloidosis
Author(s) -
Haan J.,
MaatSchieman M. L. C.,
Duinen S. G.,
Jensson O.,
Thorsteinsson L.,
Roos R. A. C.
Publication year - 1994
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/j.1600-0404.1994.tb02648.x
Subject(s) - cerebral amyloid angiopathy , cystatin c , pathology , amyloidosis , medicine , angiopathy , amyloid (mycology) , immunostaining , cystatin , disease , immunohistochemistry , endocrinology , dementia , creatinine , diabetes mellitus
Based on the recent discovery of co‐localization of β/A4 and cystatin C in cortical blood vessels of patients with cerebral hemorrhages due to sporadic amyloid angiopathy and patients with Alzheimer's disease we investigated the presence of these two proteins in the cortical blood vessels of patients suffering from hereditary cerebral hemorrhage with amyioidosis of the Dutch (n = 11) and the Icelandic (n = 2) type. The brains of three patients with sporadic cerebral amyloid angiopathy were also investigated. Blood vessels of the Dutch patients clearly showed immunostaining with β/A4 as well as with cystatin C antibodies, whereas the blood vessels of Icelandic patients showed only staining with cystatin C. In one of the three sporadic amyloid angiopathy patients co‐localization was shown as well. The co‐localization of mutated β/A4 with normal cystatin C in the Dutch patients suggests that cystatin C deposition occurs secondarily to β/A4 deposition. This is probably also the case in sporadic amyloid angiopathy and Alzheimer's disease. Cystatin C deposition may play a role in the development of cerebral hemorrhages and leukoencephalopathy.