Amyloid β-protein length and cerebral amyloid angiopathy-related haemorrhage

被引:20
作者
McCarron, MO [1 ]
Nicoll, JAR
Stewart, J
Cole, GM
Yang, FS
Ironside, JW
Mann, DMA
Love, S
Graham, DI
机构
[1] So Gen Hosp, Inst Neurol Sci, Dept Neuropathol, Glasgow G51 4TF, Lanark, Scotland
[2] So Gen Hosp, Inst Neurol Sci, Dept Neurol, Glasgow G51 4TF, Lanark, Scotland
[3] Univ Calif Los Angeles, Dept Med, Los Angeles, CA 91343 USA
[4] Sepulveda VAMC, Los Angeles, CA 91343 USA
[5] Univ Edinburgh, Western Gen Hosp, Dept Pathol, Neuropathol Lab, Edinburgh EX4 2XU, Midlothian, Scotland
[6] Univ Manchester, Dept Pathol Sci, Manchester M13 9PT, Lancs, England
[7] Frenchay Hosp, Dept Neuropathol, Bristol BS16 1LE, Avon, England
关键词
amyloid beta-protein; apolipoprotein C; cerebral amyloid angiopathy; haemorrhage;
D O I
10.1097/00001756-200004070-00008
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The relationship between amyloid beta-prorein (A beta) length and the apolipoprotein E (APOE) epsilon 2 allele, which is over-represented in cerebral amyloid angiopathy-related haemorrhage (CAAH), has not previously been examined. Of 57 CAA patients studied, 37 had CAAH. All patients, particularly those with CAAH had more blood vessels immunoreactive for A beta 40 than A beta 42 in both the leptomeninges and cerebral cortex. CAAH patients had more A beta 40-immunoreactive blood vessels in the leptomeninges (p < 0.001) and cortex (p = 0.027) than had non-haemorrhage patients. Cortical blood vessels, the usual source of haemorrhage in CAAH, were more frequently A beta 42 immunoreactive in APOE epsilon 2 carriers than in non-epsilon 2 carriers (p=0.022). The APOE epsilon 2 allele may predispose to CAAH by increasing the seeding of cortical blood vessels by A beta 42. NeuroReport 11:937-940 (C) 2000 Lippincott Williams & Wilkins.
引用
收藏
页码:937 / 940
页数:4
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