ArticleStroke2014
Cerebral amyloid angiopathy increases susceptibility to infarction after focal cerebral ischemia in Tg2576 mice.
Article in Stroke, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
- Assessing blood-brain barrier (BBB) integrity in an Alzheimer's disease mouse model: is the BBB globally or locally disrupted?Fluids and barriers of the CNS · 2025Article
- Models and mechanisms of post-stroke dementia and cognitive impairment.Frontiers in stroke · 2025Article
- The contribution of β-amyloid, Tau and α-synuclein to blood-brain barrier damage in neurodegenerative disorders.Acta neuropathologica · 2024Review
- Multifocal Cerebral Microinfarcts Modulate Early Alzheimer's Disease Pathology in a Sex-Dependent Manner.Frontiers in immunology · 2021Article
- From Neurodevelopmental to Neurodegenerative Disorders: The Vascular Continuum.Frontiers in aging neuroscience · 2021Review
- Cerebral artery dilation during transient ischemia is impaired by amyloid β deposition around the cerebral artery in Alzheimer's disease model mice.The journal of physiological sciences : JPS · 2020Article
- From Stroke to Dementia: a Comprehensive Review Exposing Tight Interactions Between Stroke and Amyloid-β Formation.Translational stroke research · 2020Review
- Mouse models of Alzheimer's disease cause rarefaction of pial collaterals and increased severity of ischemic stroke.Angiogenesis · 2019Article
- Effects of Dabigatran in Mouse Models of Aging and Cerebral Amyloid Angiopathy.Frontiers in neurology · 2019Article
- Identification of a peptide recognizing cerebrovascular changes in mouse models of Alzheimer's disease.Nature communications · 2017Article
- Cerebral blood flow regulation and neurovascular dysfunction in Alzheimer disease.Nature reviews. Neuroscience · 2017Review
- Physiologic Reelin does not play a strong role in protection against acute stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2016Article
- The effect of Scutellaria baicalensis stem-leaf flavonoids on spatial learning and memory in chronic cerebral ischemia-induced vascular dementia of rats.Acta biochimica et biophysica Sinica · 2016Article
- Heparan sulfate proteoglycans mediate Aβ-induced oxidative stress and hypercontractility in cultured vascular smooth muscle cells.Molecular neurodegeneration · 2016Article
- Cerebral Small Vessel Disease: Targeting Oxidative Stress as a Novel Therapeutic Strategy?Frontiers in pharmacology · 2016Review
- Ischemic brain injury in cerebral amyloid angiopathy.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
background and purposeWe and others have shown that soluble amyloid β-peptide (Aβ) and cerebral amyloid angiopathy (CAA) cause significant cerebrovascular dysfunction in mutant amyloid precursor protein (APP) mice, and that these deficits are greater in aged APP mice having CAA compared with young APP mice lacking CAA. Amyloid β-peptide in young APP mice also increases infarction after focal cerebral ischemia, but the impact of CAA on ischemic brain injury is unknown.
methodsTo determine this, we assessed cerebrovascular reactivity, cerebral blood flow (CBF), and extent of infarction and neurological deficits after transient middle cerebral artery occlusion in aged APP mice having extensive CAA versus young APP mice lacking CAA (and aged-matched littermate controls).
resultsWe found that aged APP mice have more severe cerebrovascular dysfunction that is CAA dependent, have greater CBF compromise during and immediately after middle cerebral artery occlusion, and develop larger infarctions after middle cerebral artery occlusion.
conclusionsThese data indicate CAA induces a more severe form of cerebrovascular dysfunction than amyloid β-peptide alone, leading to intra- and postischemic CBF deficits that ultimately exacerbate cerebral infarction. Our results shed mechanistic light on human studies identifying CAA as an independent risk factor for ischemic brain injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.