ArticleJournal of neurotrauma2016
Altered Neuroinflammation and Behavior after Traumatic Brain Injury in a Mouse Model of Alzheimer's Disease.
Article in Journal of neurotrauma, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed.
- Article
- Traumatic Brain Injury and the Road to Alzheimer's Disease.Biomedicines · 2026Review
- Complement in Traumatic Brain Injury: Linking Acute Injury to Chronic Neurodegeneration.European journal of immunology · 2026Review
- Neuroinflammation in Alzheimer disease.Nature reviews. Immunology · 2025Review
- Adolescent mice exposed to TBI developed PD-like pathology in middle age.Translational psychiatry · 2025Article
- Cerebral amyloid angiopathy: a narrative review.Frontiers in aging neuroscience · 2025Review
- Review
- Traumatic brain injury alters the effects of class II invariant peptide (CLIP) antagonism on chronic meningeal CLIP + B cells, neuropathology, and neurobehavioral impairment in 5xFAD mice.Journal of neuroinflammation · 2024Article
- Glycerophospholipid dysregulation after traumatic brain injury.Neurochemistry international · 2024Review
- Inflammasome activation in traumatic brain injury and Alzheimer's disease.Translational research : the journal of laboratory and clinical medicine · 2023Review
- Mast cell-mediated immune regulation in health and disease.Frontiers in medicine · 2023Review
- Sleep fragmentation engages stress-responsive circuitry, enhances inflammation and compromises hippocampal function following traumatic brain injury.Experimental neurology · 2022Article
- Fecal Microbiota Transplantation Derived from Alzheimer's Disease Mice Worsens Brain Trauma Outcomes in Wild-Type Controls.International journal of molecular sciences · 2022Article
- Lateral Fluid Percussion Injury Causes Sex-Specific Deficits in Anterograde but Not Retrograde Memory.Frontiers in behavioral neuroscience · 2022Article
- Triggering receptor expressed on myeloid cells 2 deficiency exacerbates injury-induced inflammation in a mouse model of tauopathy.Frontiers in immunology · 2022Article
- The Emergence of Model Systems to Investigate the Link Between Traumatic Brain Injury and Alzheimer's Disease.Frontiers in aging neuroscience · 2021Review
- miR-146a Mimics Ameliorates Traumatic Brain Injury Involving JNK and NF-κB Signaling Pathway.Neuromolecular medicine · 2020Article
- Sleep Disruption Exacerbates and Prolongs the Inflammatory Response to Traumatic Brain Injury.Journal of neurotrauma · 2020Article
- Brain Injury-Mediated Neuroinflammatory Response and Alzheimer's Disease.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2020Review
- Activation of mGluR1 Mediates C1q-Dependent Microglial Phagocytosis of Glutamatergic Synapses in Alzheimer's Rodent Models.Molecular neurobiology · 2019Article
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
Traumatic brain injury (TBI) has acute and chronic sequelae, including an increased risk for the development of Alzheimer's disease (AD). TBI-associated neuroinflammation is characterized by activation of brain-resident microglia and infiltration of monocytes; however, recent studies have implicated beta-amyloid as a major manipulator of the inflammatory response. To examine neuroinflammation after TBI and development of AD-like features, these studies examined the effects of TBI in the presence and absence of beta-amyloid. The R1.40 mouse model of cerebral amyloidosis was used, with a focus on time points well before robust AD pathologies. Unexpectedly, in R1.40 mice, the acute neuroinflammatory response to TBI was strikingly muted, with reduced numbers of CNS myeloid cells acquiring a macrophage phenotype and decreased expression of inflammatory cytokines. At chronic time points, macrophage activation substantially declined in non-Tg TBI mice; however, it was relatively unchanged in R1.40 TBI mice. The persistent inflammatory response coincided with significant tissue loss between 3 and 120 days post-injury in R1.40 TBI mice, which was not observed in non-Tg TBI mice. Surprisingly, inflammatory cytokine expression was enhanced in R1.40 mice compared with non-Tg mice, regardless of injury group. Although R1.40 TBI mice demonstrated task-specific deficits in cognition, overall functional recovery was similar to non-Tg TBI mice. These findings suggest that accumulating beta-amyloid leads to an altered post-injury macrophage response at acute and chronic time points. Together, these studies emphasize the role of post-injury neuroinflammation in regulating long-term sequelae after TBI and also support recent studies implicating beta-amyloid as an immunomodulator.
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