ArticleJournal of Alzheimer's disease : JAD2021
Cerebral Amyloid Angiopathy in a Mouse Model of Alzheimer's Disease Associates with Upregulated Angiopoietin and Downregulated Hypoxia-Inducible Factor.
Article in Journal of Alzheimer's disease : JAD, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Heterogenous microglial reactivity contrasts with stable vascular transcriptional programs in mouse models of Alzheimer's, CADASIL, and Traumatic Brain Injury.Nature communications · 2026Article
- Development of Plasma Protein Classification Models for Alzheimer's Disease Using Multiple Machine Learning Approaches.International journal of molecular sciences · 2025Article
- Cerebral amyloid angiopathy: a narrative review.Frontiers in aging neuroscience · 2025Review
- Models and mechanisms of post-stroke dementia and cognitive impairment.Frontiers in stroke · 2025Article
- Reduction of Microvessel Number and Length in the Cerebellum of Purkinje Cell Degeneration Mice.Cerebellum (London, England) · 2024Article
- Beta-Amyloid Enhances Vessel Formation in Organotypic Brain Slices Connected to Microcontact Prints.Biomolecules · 2023Article
- High affinity of β-amyloid proteins to cerebral capillaries: implications in chronic lead exposure-induced neurotoxicity in rats.Fluids and barriers of the CNS · 2023Article
- Impaired astrocytic CaeLife · 2022Article
- Multi-omics analysis revealed the role of CCT2 in the induction of autophagy in Alzheimer's disease.Frontiers in genetics · 2022Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundVascular pathology is a common feature in patients with advanced Alzheimer's disease, with cerebral amyloid angiopathy (CAA) and microvascular changes commonly observed at autopsies and in genetic mouse models. However, despite a plethora of studies addressing the possible impact of CAA on brain vasculature, results have remained contradictory, showing reduced, unchanged, or even increased capillary densities in human and rodent brains overexpressing amyloid-β in Alzheimer's disease and Down's syndrome.
objectiveWe asked if CAA is associated with changes in angiogenetic factors or receptors and if so, whether this would translate into morphological alterations in pericyte coverage and vessel density.
methodsWe utilized the transgenic mice carrying the Arctic (E693G) and Swedish (KM670/6701NL) amyloid precursor protein which develop severe CAA in addition to parenchymal plaques.
resultsThe main finding of the present study was that CAA in Tg-ArcSwe mice is associated with upregulated angiopoietin and downregulated hypoxia-inducible factor. In the same mice, we combined immunohistochemistry and electron microscopy to quantify the extent of CAA and investigate to which degree vessels associated with amyloid plaques were pathologically affected. We found that despite a severe amount of CAA and alterations in several angiogenetic factors in Tg-ArcSwe mice, this was not translated into significant morphological alterations like changes in pericyte coverage or vessel density.
conclusionOur data suggest that CAA does not impact vascular density but might affect capillary turnover by causing changes in the expression levels of angiogenetic factors.
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