ArticleInternational journal of molecular sciences2021
Repetitive Traumatic Brain Injury Causes Neuroinflammation before Tau Pathology in Adolescent P301S Mice.
Article in International journal of molecular sciences, 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.
- Nasal anti-CD3 monoclonal antibody ameliorates traumatic brain injury, enhances microglial phagocytosis and reduces neuroinflammation via IL-10-dependent TNature neuroscience · 2025Article
- Visual Impairment in Pre-Clinical Models of Mild Traumatic Brain Injury.Journal of neurotrauma · 2024Review
- Concussion burden and later-life cardiovascular risk factors in former professional American-style football players.Annals of clinical and translational neurology · 2024Article
- Post-stroke cognitive impairment: exploring molecular mechanisms and omics biomarkers for early identification and intervention.Frontiers in molecular neuroscience · 2024Review
- Neuronal tau pathology worsens late-phase white matter degeneration after traumatic brain injury in transgenic mice.Acta neuropathologica · 2023Article
- A Projectile Concussive Impact Model Produces Neuroinflammation in Both Mild and Moderate-Severe Traumatic Brain Injury.Brain sciences · 2023Article
- Role of microglia in HIV-1 infection.AIDS research and therapy · 2023Review
- Crry silencing alleviates Alzheimer's disease injury by regulating neuroinflammatory cytokines and the complement system.Neural regeneration research · 2022Article
- Review
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Repetitive closed head injury (rCHI) is commonly encountered in young athletes engaged in contact and collision sports. Traumatic brain injury (TBI) including rCHI has been reported to be an important risk factor for several tauopathies in studies of adult humans and animals. However, the link between rCHI and the progression of tau pathology in adolescents remains to be elucidated. We evaluated whether rCHI can trigger the initial acceleration of pathological tau in adolescent mice and impact the long-term outcomes post-injury. To this end, we subjected adolescent transgenic mice expressing the P301S tau mutation to mild rCHI and assessed tau hyperphosphorylation, tangle formation, markers of neuroinflammation, and behavioral deficits at 40 days post rCHI. We report that rCHI did not accelerate tau pathology and did not worsen behavioral outcomes compared to control mice. However, rCHI induced cortical and hippocampal microgliosis and corpus callosum astrocytosis in P301S mice by 40 days post-injury. In contrast, we did not find significant microgliosis or astrocytosis after rCHI in age-matched WT mice or sham-injured P301S mice. Our data suggest that neuroinflammation precedes the development of Tau pathology in this rCHI model of adolescent repetitive mild TBI.
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