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Neurology 2000;54:242
© 2000 American Academy of Neurology
Brief Communications

Absence of cystatin C mutation in sporadic cerebral amyloid angiopathy–related hemorrhage

M. O. McCarron, MA, MRCP, J. A. R. Nicoll, MD, FRCPath, J. Stewart, J. W. Ironside, FRCPath, D. M. A. Mann, PhD, FRCPath, S. Love, PhD, FRCP, FRCPath, D. I. Graham, PhD, FRCPath and A. Grubb, MD, PhD

From the Departments of Neurology (Dr. McCarron) and Neuropathology (Drs. McCarron, Nicoll, Graham, and J. Stewart), Institute of Neurological Sciences, Southern General Hospital, Glasgow, UK; Neuropathology Laboratory (Dr. Ironside), Department of Pathology, the University of Edinburgh, Western General Hospital, Edinburgh, UK; Department of Pathological Sciences (Dr. Mann), University of Manchester, UK; Department of Neuropathology (Dr. Love), Frenchay Hospital, Bristol, UK; and Department of Clinical Chemistry (Dr. Grubb), University of Lund, University Hospital, Sweden.

Address correspondence and reprint requests to Dr. Mark O. McCarron, Department of Neuropathology, Institute of Neurological Sciences, Southern General Hospital, Glasgow G51 4TF, UK.

In Icelandic pedigrees a cystatin C mutation, glutamine 68 (L68Q), causes autosomal dominant cerebral amyloid angiopathy–related hemorrhage (CAAH). We examined 33 patients with sporadic CAAH for this mutation. None carried L68Q and, including this report, only one of 52 published cases of sporadic CAAH has had the cystatin C mutation. Despite vascular colocalization of cystatin C with amyloid ß-protein, cystatin C L68Q is rare in sporadic CAAH.

Key words: Cerebral amyloid angiopathy—Intracerebral hemorrhage—Cystatin C






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