Progression of Cerebral Amyloid Angiopathy: Accumulation of Amyloid-β40 in Affected Vessels

作者: Norma C. Alonzo , Bradley T. Hyman , G William Rebeck , Steven M. Greenberg

DOI: 10.1097/00005072-199804000-00008

关键词: Apolipoprotein EPathogenesisCerebral amyloid angiopathyCentral nervous system diseaseAmyloidosisVascular diseaseAsymptomaticAmyloidPathologyMedicine

摘要: Cerebrovascular deposits of amyloid (cerebral angiopathy, or CAA) are generally asymptomatic, but in advanced cases, they can lead to vessel rupture and hemorrhage. The process progression CAA was studied by comparison postmortem brains with asymptomatic ("mild") the form disease associated hemorrhage ("severe CAA"). Cortical meningeal vessels were immunostained for beta-amyloid examined confocal microscopy systematic quantitative sampling. We focused on 2 parameters: proportion affected (a measure seeding vessels) amount per growth existing lesions). Surprisingly, there no difference between cortical mild severe (0.29 vs 0.32, p = 0.65), rather an increase area 40 amino acid (198.5 +/- 38.7 455.8 100.9 microm2/vessel, < 0.007). Increasing doses (from 0 1 copies) apolipoprotein E epsilon4 allele also greater without change within each class severity. These findings suggest that from reflects progressive accumulation previously seeded amyloid, this is selectively enhanced epsilon4.

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