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APOE gene polymorphism as a risk factor for cerebral amyloid angiopathy-related hemorrhage

Nicoll, J.A. and McCarron, M.O. (2001) APOE gene polymorphism as a risk factor for cerebral amyloid angiopathy-related hemorrhage Amyloid: The Journal of Protein Folding Disorders, 8, (1), pp. 51-55.

Record type: Article


Cerebral amyloid angiopathy (CAA) due to the accumulation of amyloid beta-protein (Abeta) occurs in up to half of elderly individuals and in most cases of Alzheimer's disease (AD). Following identification of the apolipoprotein E (APOE) epsilon4 allele as a risk factor for AD, APOE epsilon4 was also found to be associated with asymptomatic CAA. The major clinical manifestation of CAA is stroke due to a lobar hemorrhage. A complex relationship between APOE epsilon4, APOE epsilon2 and hemorrhage associated with CAA (CAAH) is emerging. Pathological studies have demonstrated that APOE epsilon2 is over-represented among patients with CAAH. This remains the case for patients with co-existing Alzheimer's disease, who otherwise have a very low epsilon2 allele frequency. Other forms of intracranial hemorrhage do not share the same association, indicating that APOE epsilon2 has a specific association with CAAH. Patients with the epsilon2 allele and CAAH are more likely to have taken anticoagulant or antiplatelet medication, had hypertension or had minor head trauma than non-epsilon2 carriers. In addition, the epsilon2 allele is specifically associated with CAA-associated microangiopathic changes such as fibrinoid necrosis and concentric splitting of the vessel wall.

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Published date: 2001


Local EPrints ID: 27671
ISSN: 1350-6129
PURE UUID: d817c7dd-4d26-462f-b92e-61ede140a868
ORCID for J.A. Nicoll: ORCID iD

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Date deposited: 27 Apr 2006
Last modified: 17 Jul 2017 16:04

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