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Cited by 138Alzheimer's disease research and treatmentsIntracerebral and Subarachnoid Hemorrhage ResearchNeurological Disease Mechanisms and Treatments

Capillary cerebral amyloid angiopathy is associated with vessel occlusion and cerebral blood flow disturbances

Thal, Dietmar Rudolf, Capetillo-Zarate, Estibaliz, Larionov, Sergey, Staufenbiel, Matthias, Zurbruegg, Stefan, Beckmann, Nicolau·2009·Neurobiology of Aging
DOI 10.1016/j.neurobiolaging.2008.01.017
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Abstract

The role of cerebral amyloid angiopathy (CAA) in the pathogenesis of Alzheimer's disease (AD) is not fully understood. Here, we studied whether CAA is associated with alterations in microvascularisation in transgenic mouse models and in the human brain. APP23 mice at 25-26 months of age exhibited severe CAA in thalamic vessels whereas APP51/16 mice did not. Wild-type littermates were free of CAA. We found CAA-related capillary occlusion within the thalamus of APP23 mice but not in APP51/16 and wild-type mice. Magnetic resonance angiography (MRA) showed blood flow alterations in the thalamic vessels of APP23 mice. CAA-related capillary occlusion in the branches of the thalamoperforating arteries of APP23 mice, thereby, corresponded to the occurrence of blood flow disturbances. Similarly, CAA-related capillary occlusion was observed in the human occipital cortex of AD cases but less frequently in controls. These results indicate that capillary CAA can result in capillary occlusion and is associated with cerebral blood flow disturbances providing an additional mechanism for toxic effects of the amyloid beta-protein in AD.

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  • VAβ is detrimental to the function of cerebrovascular circulation through compromising blood-brain-barrier integrity, effecting hemodynamic dysfunction, and facilitating occurrence of spontaneous hemorrhages.

    “VAβ is detrimental to the function of cerebrovascular circulation through compromising blood–brain-barrier integrity [49], effecting hemodynamic dysfunction [29, 50], and facilitating occurrence of spontaneous hemorrhages [25, 26, 36].”

    From APOE Genotype Differentially Modulates Effects of Anti-Aβ, Passive Immunization in APP Transgenic Mice (2017) · cites this paper as [29]

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Authors
Thal, D. R., Capetillo-Zarate, E., Larionov, S., Staufenbiel, M., Zurbruegg, S., & Beckmann, N.
Affiliations
  • University of Bonn (DE)
  • Novartis (Switzerland) (CH)
Corresponding author
Thal, Dietmar Rudolf
ORCID
Venue
Neurobiology of Aging
Publisher
Elsevier BV
Published
2009-12
Volume
30
Issue
12
Pages
1936-1948
ISSN
0197-4580 (ISSN-L)
DOI
10.1016/j.neurobiolaging.2008.01.017
OpenAlex
W1994609866
Cited by
138
References
67
Citations by year
2026: 3 · 2025: 5 · 2024: 5 · 2023: 3 · 2022: 13 · 2021: 14 · 2020: 5 · 2019: 6 · 2018: 6 · 2017: 6 · 2016: 9 · 2015: 7 · 2014: 8 · 2013: 9 · 2012: 10
FWCI
6.56
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Neurobiology of Aging (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Chinese Academy of Agricultural Sciences
  • Novartis Institutes for BioMedical Research
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Neurology › Intracerebral and Subarachnoid Hemorrhage Research
  • Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Keywords
cerebral amyloid angiopathy, capillary occlusion, cerebral blood flow, Alzheimer's disease, APP23 mice, thalamus, amyloid-beta, microvascular dysfunction, occipital cortex, transgenic mouse model
MeSH terms
Adult, Aged, Aged, 80 and over, Alzheimer Disease, Animals, Brain, Capillaries, Cerebrovascular Circulation, Disease Models, Animal, Female, Humans, Male, Mice, Inbred C57BL, Mice, Transgenic, Middle Aged, Occipital Lobe, Species Specificity, Thalamus, Cerebral Amyloid Angiopathy, Mice, Microvessels

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