Characteristics of Dyshoric Capillary Cerebral Amyloid Angiopathy
Abstract
Cerebral amyloid angiopathy (CAA) affects brain parenchymal and leptomeningeal arteries and arterioles but sometimes involves capillaries (capCAA) with spread of the amyloid into the surrounding neuropil, that is, dyshoric changes. We determined the relationship between capCAA and larger vessel CAA, β amyloid (Aβ) plaques, neurofibrillary changes, inflammation, and apolipoprotein E (APOE) in 22 cases of dyshoric capCAA using immunohistochemistry. The dyshoric changes contained predominantly Aβ1-40, whereas dense bulblike deposits adjacent to the capillary wall contained mostly Aβ1-42. There was an inverse local correlation between Aβ plaque load and capCAA severity (p = 0.01), suggesting that Aβ transport between the neuropil and the circulation may be mechanistically involved. Deposits of hyperphosphorylated tau and ubiquitin and clusters of activated microglia, resembling the changes around Aβ plaques, were found around capCAA but were absent around larger vessel CAA. In 14 cases for which APOE genotype was available, there was a high APOE-ε4 allele frequency (54%; 43% homozygous). The severity of CapCAA increased with the number of ε4-alleles; and APOE4 seemed to colocalize with capCAA by immunohistochemistry. These results suggest that capCAA is pathologically and possibly pathogenetically distinct from larger vessel CAA, and that it is associated with a high APOE-ε4 allele frequency.
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Previous immunohistochemical studies in AD patients and in a transgenic rat model of CAA have found that CAA type 1, i.e., amyloid deposition in the capillary vessels, was associated with perivascular inflammation.
“On the other hand, previous immunohistochemical studies in AD patients and in a transgenic rat model of CAA have found that CAA type 1, i.e., amyloid deposition in the capillary vessels, was associated with perivascular inflammation [39, 40].”
From Cerebrospinal fluid levels of the neurotrophic factor neuroleukin are increased in early Alzheimer’s disease, but not in cerebral amyloid angiopathy (2021) · cites this paper as [40]
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- Authors
- Richard, E., Carrano, A., Hoozemans, J. J., van Horssen, J., van Haastert, E. S., Eurelings, L. S., de Vries, H. E., Thal, D. R., Eikelenboom, P., van Gool, W. A., & Rozemuller, A. J. M.
- Affiliations
- Amsterdam UMC Location University of Amsterdam (NL)
- Amsterdam Neuroscience (NL)
- Venue
- Journal of Neuropathology & Experimental Neurology
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-11
- Volume
- 69
- Issue
- 11
- Pages
- 1158-1167
- ISSN
- 0022-3069 (ISSN-L)
- 1554-6578
- OpenAlex
- W2034297743
- Cited by
- 71
- References
- 5
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 4 · 2023: 3 · 2022: 8 · 2021: 12 · 2020: 4 · 2019: 2 · 2018: 6 · 2017: 1 · 2016: 2 · 2015: 5 · 2014: 5 · 2013: 5 · 2012: 4
- FWCI
- 2.67
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neuropathology & Experimental Neurology (publishedVersion)
- PubMed (publishedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Digital Academic REpository of VU University Amsterdam (Vrije Universiteit Amsterdam) (submittedVersion)
- Pure Amsterdam UMC (submittedVersion)
- Topics
- Health Sciences › Medicine › Neurology › Intracerebral and Subarachnoid Hemorrhage Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Neurology › Cerebrovascular and genetic disorders
- Keywords
- cerebral amyloid angiopathy, amyloid-beta, APOE ε4, hyperphosphorylated tau, ubiquitin, microglial activation, neuroinflammation
- MeSH terms
- Aged, Aged, 80 and over, Brain, Capillaries, Female, Glial Fibrillary Acidic Protein, HLA-DR Antigens, Humans, Male, Meningeal Arteries, Amyloid beta-Peptides, Cerebral Amyloid Angiopathy, tau Proteins, Ubiquitin, Apolipoprotein E4
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