ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2014
Juvenile traumatic brain injury induces long-term perivascular matrix changes alongside amyloid-beta accumulation.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Eicosapentaenoic acid reprograms cerebrovascular metabolism and impairs repair after brain injury, with relevance to chronic traumatic encephalopathy.Cell reports · 2026Article
- Traumatic Brain Injury and Alzheimer's Disease: A Shared Neurovascular Hypothesis.Neuroscience insights · 2025Review
- Exploring Heparan Sulfate Proteoglycans as Mediators of Human Mesenchymal Stem Cell Neurogenesis.Cellular and molecular neurobiology · 2024Review
- Immune-Neurovascular Interactions in Experimental Perinatal and Childhood Arterial Ischemic Stroke.Stroke · 2024Review
- Brain Maturation as a Fundamental Factor in Immune-Neurovascular Interactions in Stroke.Translational stroke research · 2024Review
- A single mild juvenile TBI in male mice leads to regional brain tissue abnormalities at 12 months of age that correlate with cognitive impairment at the middle age.Acta neuropathologica communications · 2023Article
- The role of SUMOylation in the neurovascular dysfunction after acquired brain injury.Frontiers in pharmacology · 2023Review
- Fetal glucocorticoid exposure leads to sex-specific changes in drug-transporter function at the blood-brain barrier in juvenile guinea pigs.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Pediatric Traumatic Brain Injury: An Update on Preclinical Models, Clinical Biomarkers, and the Implications of Cerebrovascular Dysfunction.Journal of central nervous system disease · 2022Review
- Microglia-leucocyte axis in cerebral ischaemia and inflammation in the developing brain.Acta physiologica (Oxford, England) · 2021Review
- Neutrophil-specific deletion of Syk results in recruitment-independent stabilization of the barrier and a long-term improvement in cognitive function after traumatic injury to the developing brain.Neurobiology of disease · 2021Article
- Multiple Particle Tracking Detects Changes in Brain Extracellular Matrix and Predicts Neurodevelopmental Age.ACS nano · 2021Article
- Neuroinflammation and Hypothalamo-Pituitary Dysfunction: Focus of Traumatic Brain Injury.International journal of molecular sciences · 2021Review
- Review of Alterations in Perlecan-Associated Vascular Risk Factors in Dementia.International journal of molecular sciences · 2020Review
- Article
- CX3CR1-CCR2-dependent monocyte-microglial signaling modulates neurovascular leakage and acute injury in a mouse model of childhood stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019Article
- Brain-Immune Interactions and Neuroinflammation After Traumatic Brain Injury.Frontiers in neuroscience · 2019Review
- Fibronectin induces the perivascular deposition of cerebrospinal fluid-derived amyloid-β in aging and after stroke.Neurobiology of aging · 2018Article
- Military-related risk factors for dementia.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2018Review
- Cerebrovascular contribution to dementia development after traumatic brain injury: promises and problems.Annals of translational medicine · 2018Article
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Authors and funding
7 authors.
Funding
Abstract
In our juvenile traumatic brain injury (jTBI) model, emergence of cognitive dysfunctions was observed up to 6 months after trauma. Here we hypothesize that early brain injury induces changes in the neurovascular unit (NVU) that would be associated with amyloid-beta (Aβ) accumulation. We investigated NVU changes for up to 6 months in a rat jTBI model, with a focus on the efflux protein P-glycoprotein (P-gp) and on the basement membrane proteins perlecan and fibronectin, all known to be involved in Aβ clearance. Rodent-Aβ staining is present and increased after jTBI around cerebral blood microvessels, and the diameter of those is decreased by 25% and 34% at 2 and 6 months, respectively, without significant angiogenesis. P-glycoprotein staining in endothelium is decreased by 22% and parallels an increase of perlecan and fibronectin staining around cerebral blood vessels. Altogether, these results strongly suggest that the emergence of long-term behavioral dysfunctions observed in rodent jTBI may be related to endothelial remodeling at the blood-brain barrier alongside vascular dysfunction and altered Aβ trafficking. This study shows that it is important to consider jTBI as a vascular disorder with long-term consequences on cognitive functions.
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