ArticleFrontiers in aging neuroscience2016
Development of Cerebral Microbleeds in the APP23-Transgenic Mouse Model of Cerebral Amyloid Angiopathy-A 9.4 Tesla MRI Study.
Article in Frontiers in aging neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 28 citations in OpenAlex.
- Aβ1-40 induces venular endothelial cell ferroptosis in cerebral amyloid angiopathy via the ATF3/xCT axis: Insights from single-cell RNA sequencing.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Type I interferon drives T cell responses to amyloid beta in the central nervous system.Nature communications · 2026Article
- Review
- Vasomotion loss precedes impaired cerebrovascular reactivity and microbleeds in cerebral amyloid angiopathy.Brain communications · 2025Article
- The presence of circulating human apolipoprotein J reduces the occurrence of cerebral microbleeds in a transgenic mouse model with cerebral amyloid angiopathy.Alzheimer's research & therapy · 2024Article
- Age-Associated Changes in Endothelial Transcriptome and Epigenetic Landscapes Correlate With Elevated Risk of Cerebral Microbleeds.Journal of the American Heart Association · 2023Article
- Cortical cerebrovascular and metabolic perturbations in the 5xFAD mouse model of Alzheimer's disease.Frontiers in aging neuroscience · 2023Article
- Transcriptional signature in microglia isolated from an Alzheimer's disease mouse model treated with scanning ultrasound.Bioengineering & translational medicine · 2023Article
- Blood-brain barrier leakage in Alzheimer's disease: From discovery to clinical relevance.Pharmacology & therapeutics · 2022Review
- Impact of Cerebral Amyloid Angiopathy in Two Transgenic Mouse Models of Cerebral β-Amyloidosis: A Neuropathological Study.International journal of molecular sciences · 2022Article
- Dysfunction of the Blood-brain Barrier in Cerebral Microbleeds: from Bedside to Bench.Aging and disease · 2021Review
- In vivo characterization of spontaneous microhemorrhage formation in mice with cerebral amyloid angiopathy.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- The brains of aged mice are characterized by altered tissue diffusion properties and cerebral microbleeds.Journal of translational medicine · 2020Article
- Sub-acute Cerebral Microhemorrhages Induced by Lipopolysaccharide Injection in Rats.Journal of visualized experiments : JoVE · 2018Article
- Review
- Safety and Efficacy of Scanning Ultrasound Treatment of Aged APP23 Mice.Frontiers in neuroscience · 2018Article
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Authors and funding
8 authors at 4 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundCerebral amyloid angiopathy (CAA) is characterized by extracellular deposition of amyloid β (Aβ) around cerebral arteries and capillaries and leads to an increased risk for vascular dementia, spontaneous lobar hemorrhage, convexal subarachnoid hemorrhage, and transient focal neurological episodes, which might be an indicator of imminent spontaneous intracerebral hemorrhage. In CAA cerebral microbleeds (cMBs) with a cortical/juxtacortical distribution are frequently observed in standard magnetic resonance imaging (MRI). In vivo MRI of transgenic mouse models of CAA may serve as a useful tool to investigate translational aspects of the disease. MATERIALS AND
methodsAPP23-transgenic mice demonstrate cerebrovascular Aβ deposition with subsequent neuropathological changes characteristic for CAA. We performed a 9.4 Tesla high field MRI study using T2, T2* and time of flight-magnetic resonance angiograpy (TOF-MRA) sequences in APP23-transgenic mice and wildtype (wt) littermates at the age of 8, 12, 16, 20 and 24 months, respectively. Numbers, size, and location of cMBs are reported.
resultsT2* imaging demonstrated cMBs (diameter 50-300 μm) located in the neocortex and, to a lesser degree, in the thalamus. cMBs were detected at the earliest at 16 months of age. Numbers increased exponentially with age, with 2.5 ± 2 (median ± interquartilrange) at 16 months, 15 ± 6 at 20 months, and 31.5 ± 17 at 24 months of age, respectively.
conclusionWe report the temporal and spatial development of cMBs in the aging APP23-transgenic mouse model which develops characteristic pathological patterns known from human CAA. We expect this mouse model to serve as a useful tool to non-invasively monitor mid- and longterm translational aspects of CAA and to investigate experimental therapeutic strategies in longitudinal studies.
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