AI Article Synopsis
- CAA (Cerebral Amyloid Angiopathy) typically doesn't show symptoms but can lead to severe issues like hemorrhage in advanced cases.
- A study comparing postmortem brains with mild vs. severe CAA found no significant difference in the percentage of affected cortical vessels, but a notable increase in amyloid deposits in severe cases.
- The presence of the apolipoprotein E epsilon4 allele appears to amplify the accumulation of amyloid in vessels, indicating that progression of CAA is linked to the buildup of amyloid in previously affected vessels.
Article Abstract
Cerebrovascular deposits of amyloid (cerebral amyloid angiopathy, or CAA) are generally asymptomatic, but in advanced cases, they can lead to vessel rupture and hemorrhage. The process of progression in CAA was studied by comparison of postmortem brains with asymptomatic ("mild") CAA to brains with the form of the disease associated with hemorrhage ("severe CAA"). Cortical and meningeal vessels were immunostained for beta-amyloid and examined by confocal microscopy and by systematic quantitative sampling. We focused on 2 quantitative parameters: the proportion of vessels affected by amyloid (a measure of amyloid seeding of vessels) and the amount of amyloid per affected vessel (a measure of growth of existing lesions). Surprisingly, there was no difference between the proportion of affected cortical vessels in mild and severe CAA (0.29 vs 0.32, p = 0.65), but rather an increase in the area of the 40 amino acid form of beta-amyloid per affected cortical vessel (198.5 +/- 38.7 vs 455.8 +/- 100.9 microm2/vessel, p < 0.007). Increasing doses (from 0 to 1 to 2 copies) of the apolipoprotein E epsilon4 allele were also associated with greater amyloid per vessel without change in the proportion of affected vessels within each class of CAA severity. These findings suggest that progression from asymptomatic to advanced CAA reflects progressive accumulation of amyloid in vessels previously seeded with amyloid, and that this process is selectively enhanced by apolipoprotein E epsilon4.
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| http://dx.doi.org/10.1097/00005072-199804000-00008 | DOI Listing |
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