ArticleFrontiers in neuroscience2020
Persistent Neurovascular Unit Dysfunction: Pathophysiological Substrate and Trigger for Late-Onset Neurodegeneration After Traumatic Brain Injury.
Article in Frontiers in neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- The glymphatic-lymphatic axis: known pathways, open questions, and emerging roles in neurodegeneration.Translational neurodegeneration · 2026Review
- Individual 18F-FDG PET and arterial spin labeling coupling based on simultaneous PET/MRI predicting anti-seizure medication response in temporal lobe epilepsy patients.European journal of nuclear medicine and molecular imaging · 2026Article
- Neurovascular coupling dysfunction of the frontal‒thalamic circuit in postconcussion syndrome.Brain imaging and behavior · 2026Article
- The predictive value of serum 25(OH)D, AQP4, and IL-4 levels for edema volume and clinical prognosis after traumatic brain injury.Frontiers in medicine · 2026Article
- U-shaped pattern in the association between serum magnesium levels and long-term dementia risk after traumatic brain injury: a retrospective cohort study.Frontiers in nutrition · 2026Article
- Neurovascular Dysfunction and Glymphatic Impairment: An Unexplored Therapeutic Frontier in Neurodegeneration.International journal of molecular sciences · 2025Review
- Social deficits mirror delayed cerebrovascular dysfunction after traumatic brain injury.Acta neuropathologica communications · 2024Article
- Inflammatory response in traumatic brain and spinal cord injury: The role of XCL1-XCR1 axis and T cells.CNS neuroscience & therapeutics · 2024Review
- Spatiotemporal profile of atrophy in the first year following moderate-severe traumatic brain injury.Human brain mapping · 2023Article
- Neurovascular unit permeability in neuroinflammatory diseases: a common pathologic and therapeutic target?Neural regeneration research · 2023Article
- Aging reduces calreticulin expression and alters spontaneous calcium signals in astrocytic endfeet of the mouse dorsolateral striatum.npj aging · 2023Article
- m6A methylation: Critical roles in aging and neurological diseases.Frontiers in molecular neuroscience · 2023Review
- Inducing Mechanical Stimuli to Tissues Grown on a Magnetic Gel Allows Deconvoluting the Forces Leading to Traumatic Brain Injury.Neurotrauma reports · 2023Article
- Advances Research in Traumatic Encephalopathy.Biomedicines · 2022Article
- Downregulation of miR-491-5p promotes neovascularization after traumatic brain injury.Neural regeneration research · 2022Article
- Dysfunction of ABC Transporters at the Surface of BBB: Potential Implications in Intractable Epilepsy and Applications of Nanotechnology Enabled Drug Delivery.Current drug metabolism · 2022Review
- Neuroprotective Effect of Physical Activity in Ischemic Stroke: Focus on the Neurovascular Unit.Frontiers in cellular neuroscience · 2022Review
- Differential Leukocyte and Platelet Profiles in Distinct Models of Traumatic Brain Injury.Cells · 2021Article
- Quantitative Imaging of Blood-Brain Barrier Permeability Following Repetitive Mild Head Impacts.Frontiers in neurology · 2021Article
- Will Sirtuins Be Promising Therapeutic Targets for TBI and Associated Neurodegenerative Diseases?Frontiers in neuroscience · 2020Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) represents one of the major causes of death worldwide and leads to persisting neurological deficits in many of the survivors. One of the most significant long-term sequelae deriving from TBI is neurodegenerative disease, which is a group of incurable diseases that impose a heavy socio-economic burden. However, mechanisms underlying the increased susceptibility of TBI to neurodegenerative disease remain elusive. The neurovascular unit (NVU) is a functional unit composed of neurons, neuroglia, vascular cells, and the basal lamina matrix. The key role of NVU dysfunction in many central nervous system diseases has been revealed. Studies have proved the presence of prolonged structural and functional abnormalities of the NVU after TBI. Moreover, growing evidence suggests impaired NVU function is also implicated in neurodegenerative diseases. Therefore, we propose the Neurovascular Unit Dysfunction (NVUD) Hypothesis, in which the persistent NVU dysfunction is thought to underlie the development of post-TBI neurodegeneration. We deduce NVUD Hypothesis through relational inference and supporting evidence, and suggest continued NVU abnormalities following TBI serve as the pathophysiological substrate and trigger yielding chronic neuroinflammation, proteinopathies and oxidative stress, consequently leading to the progression of neurodegenerative diseases. The NVUD Hypothesis may provide potential treatment and prevention strategies for TBI and late-onset neurodegenerative diseases.
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