Cerebral amyloid angiopathy and its relationship to Alzheimer’s disease
Abstract
Cerebral amyloid angiopathy (CAA) is characterized by the deposition of the amyloid beta-protein (A beta) within cerebral vessels. The involvement of different brain areas in CAA follows a hierarchical sequence similar to that of Alzheimer-related senile plaques. Alzheimer's disease patients frequently exhibit CAA. The expansion of CAA in AD often shows the pattern of full-blown CAA. The deposition of A beta within capillaries distinguishes two types of CAA. One with capillary A beta-deposition is characterized by a strong association with the apolipoprotein E (APOE) epsilon 4 allele and by its frequent occurrence in Alzheimer's disease cases whereas the other one lacking capillary A beta-deposits is not associated with APOE epsilon 4. Capillary CAA can be seen in every stage of CAA or AD-related A beta-deposition. AD cases with capillary CAA show more widespread capillary A beta-deposition than non-demented cases as well as capillary occlusion. In a mouse model of CAA, capillary CAA was associated with capillary occlusion and cerebral blood flow disturbances. Thus, blood flow alterations with subsequent hypoperfusion induced by CAA-related capillary occlusion presumably point to a second mechanism in which A beta adversely affects the brain in AD in addition to its direct neurotoxic effects.
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In these studies ε3 allele carriers and in particular ε3 allele homozygotes constituted the largest percentage among CAA/CCA free cases.
“In these studies ε3 allele carriers and in particular ε3 allele homozygotes constituted the largest percentage among CAA/CCA free cases.”
From APOE Genotype Differentially Modulates Effects of Anti-Aβ, Passive Immunization in APP Transgenic Mice (2017) · cites this paper as [42]
Both CAA and CCA variants of VAβ pathology have been described in AD autopsies and their relative preponderance has been linked to various APOE genotypes.
“Both CAA and CCA variants of VAβ pathology have been described in AD autopsies and their relative preponderance has been linked to various APOE genotypes [40–43].”
From APOE Genotype Differentially Modulates Effects of Anti-Aβ, Passive Immunization in APP Transgenic Mice (2017) · cites this paper as [42]
Both development of CAA and CCA is primarily driven by neuron derived Aβ, while Aβ produced by myocytes locally in the tunica media further contributes to CAA development.
“Both development of CAA and CCA is primarily driven by neuron derived Aβ, while Aβ produced by myocytes locally in the tunica media further contributes to CAA development (reviewed in [42]).”
From APOE Genotype Differentially Modulates Effects of Anti-Aβ, Passive Immunization in APP Transgenic Mice (2017) · cites this paper as [42]
The largest percentage of AD patients with both CAA and CCA was found among ε4 allele carriers, while CAA without CCA was more frequent among ε2 and ε3 carriers.
“The largest percentage of AD patients with both CAA and CCA was found among ε4 allele carriers, while CAA without CCA was more frequent among ε2 and ε3 carriers [40, 42].”
From APOE Genotype Differentially Modulates Effects of Anti-Aβ, Passive Immunization in APP Transgenic Mice (2017) · cites this paper as [42]
Mechanisms underlying VAβ deposition including preferential development of CAA and CCA likely are a resultant of multiple genetic features extending beyond APOE genotype.
“They likely are a resultant of multiple genetic features extending beyond APOE genotype as no APOE allelic variant confers absolute protection against VAβ deposition [42, 43].”
From APOE Genotype Differentially Modulates Effects of Anti-Aβ, Passive Immunization in APP Transgenic Mice (2017) · cites this paper as [42]
No APOE allelic variant confers absolute protection against VAβ deposition.
“They likely are a resultant of multiple genetic features extending beyond APOE genotype as no APOE allelic variant confers absolute protection against VAβ deposition [42, 43].”
From APOE Genotype Differentially Modulates Effects of Anti-Aβ, Passive Immunization in APP Transgenic Mice (2017) · cites this paper as [42]
Cerebral amyloid angiopathy (CAA) is very commonly observed in cases with parenchymal Aβ plaques.
“Although cerebral amyloid angiopathy (CAA) is not considered in the “ABC” score, it is very commonly observed in cases with parenchymal Aβ plaques and should be evaluated and reported systematically as well as appreciated for its potential pathophysiological significance [56,61].”
From National Institute on Aging–Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach (2012) · cites this paper as [56]
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References 121 · Cited by 372
- Authors
- Thal, D. R., Griffin, W. S. T., de Vos, R. A. I., & Ghebremedhin, E.
- Affiliations
- Universität Ulm (DE)
- University of Arkansas Medical Center (US)
- Goethe University Frankfurt (DE)
- Corresponding author
- Thal, Dietmar Rudolf
- Venue
- Acta Neuropathologica
- Published
- 2008-03-28
- Volume
- 115
- Issue
- 6
- Pages
- 599-609
- ISSN
- 0001-6322 (ISSN-L)
- 1432-0533
- OpenAlex
- W2020240430
- Cited by
- 372
- References
- 121
- Citations by year
- 2026: 21 · 2025: 25 · 2024: 25 · 2023: 15 · 2022: 22 · 2021: 26 · 2020: 25 · 2019: 21 · 2018: 21 · 2017: 12 · 2016: 20 · 2015: 20 · 2014: 16 · 2013: 18 · 2012: 17
- FWCI
- 2.46
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Acta Neuropathologica (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (AG 12411, P01AG012411)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Neurology › Intracerebral and Subarachnoid Hemorrhage Research
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- cerebral amyloid angiopathy, Alzheimer's disease, amyloid-beta, APOE ε4, capillary occlusion, cerebral blood flow, cerebral hypoperfusion, amyloid plaques
- MeSH terms
- Alzheimer Disease, Amyloid, Humans, Cerebral Amyloid Angiopathy, Apolipoprotein E4
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