Publications by authors named "Taha Yahya"
Neuroinflammation plays a crucial role in traumatic brain injury (TBI), contributing to both damage and recovery, yet no effective therapy exists to mitigate central nervous system (CNS) injury and promote recovery after TBI. In the present study, we found that nasal administration of an anti-CD3 monoclonal antibody ameliorated CNS damage and behavioral deficits in a mouse model of contusional TBI. Nasal anti-CD3 induced a population of interleukin (IL)-10-producing regulatory T cells (T cells) that migrated to the brain and closely contacted microglia.
View Article and Find Full Text PDFAlzheimer's disease (AD) is the most prevalent neurodegenerative disorder. Antiamyloid antibody treatments modestly slow disease progression in mild dementia due to AD. Emerging evidence shows that homeostatic dysregulation of the brain immune system, especially that orchestrated by microglia, plays an important role in disease onset and progression.
View Article and Find Full Text PDFArticle Synopsis
- The study looked at how concussions in mice might lead to anxiety and other health problems, especially when they ate a high-salt diet.
- Mice that had concussions and then ate a high-salt diet showed increased anxiety compared to those who ate a normal diet.
- The research also found that the gut bacteria in these mice changed more with the high-salt diet than the brain injury itself, and some bacteria were linked to higher anxiety levels.
APOE4 is the strongest genetic risk factor for Alzheimer's disease (AD), with increased odds ratios in female carriers. Targeting amyloid plaques shows modest improvement in male non-APOE4 carriers. Leveraging single-cell transcriptomics across APOE variants in both sexes, multiplex flow cytometry and validation in two independent cohorts of APOE4 female carriers with AD, we identify a new subset of neutrophils interacting with microglia associated with cognitive impairment.
View Article and Find Full Text PDFTraumatic brain injury (TBI) is independently associated with hypertension and ischemic stroke. The goal of this study was to determine the interplay between TBI and incident hypertension in the occurrence of post-TBI stroke. This prospective study used a hospital-based registry to identify patients without pre-existing comorbidities.
View Article and Find Full Text PDFThe neuroimmunology of traumatic brain injury (TBI) has recently gained recognition as a crucial element in the secondary pathophysiological consequences that occur following neurotrauma. Both immune cells residing within the central nervous system (CNS) and those migrating from the periphery play significant roles in the development of secondary brain injury. However, the precise mechanisms governing communication between innate and adaptive immune cells remain incompletely understood, partly due to a limited utilization of relevant experimental models and techniques.
View Article and Find Full Text PDFTraumatic brain injury (TBI) is a leading cause of morbidity and mortality. The innate and adaptive immune responses play an important role in the pathogenesis of TBI. Gamma-delta (γδ) T cells have been shown to affect brain immunopathology in multiple different conditions, however, their role in acute and chronic TBI is largely unknown.
View Article and Find Full Text PDFArticle Synopsis
- Increased risk of cardiovascular and endocrine comorbidities after traumatic brain injury (TBI) is under-researched, particularly concerning individuals without pre-existing conditions.
- The study aimed to evaluate the incidence of various comorbidities in patients with mild (mTBI) and moderate to severe TBI (msTBI), while also investigating the relationship between these comorbidities and post-TBI mortality.
- The research included a substantial cohort of patients over a 15-year period and highlighted significant associations between TBI and an increase in cardiovascular and endocrine risks, as well as potential impacts on mortality.
Repetitive mild traumatic brain injury (mTBI) in children and adolescents leads to acute and chronic neurologic sequelae and is linked to later life neurodegenerative disease. However, the biological mechanisms connecting early life mTBI to neurodegeneration remain unknown. Using an adolescent mouse repetitive closed head injury model that induces progressive cognitive impairment in males and anxiety in females in the absence of overt histopathology, we examined transcriptional and translational changes in neurons isolated from sham and injured brain in the chronic phase after injury.
View Article and Find Full Text PDFArticle Synopsis
- - Repetitive closed head injury (rCHI) is prevalent among young athletes in contact sports and is linked to traumatic brain injury (TBI), which is associated with tauopathies in adults, but its effects on adolescents are not well understood.
- - The study used adolescent mice with a tau mutation to explore whether rCHI accelerates tau pathology, finding that while rCHI did not worsen tau or behavior, it did cause neuroinflammation in the mouse models.
- - Results indicated that rCHI led to increased microgliosis and astrocytosis in mice with the tau mutation, suggesting that neuroinflammation may occur before tau pathology in cases of adolescent repetitive mild TBI.