Journal of neurotrauma
-
Journal of neurotrauma · Feb 2017
Phase II Clinical Trial of Atorvastatin in Mild Traumatic Brain Injury.
Statins constitute a class of medications commonly used in the treatment of elevated cholesterol. However, in experimental studies, statins also have other non-cholesterol-mediated mechanisms of action, which may have neuroprotective effects. The aim of this study was to determine whether administration of atorvastatin for 7 days post-injury would improve neurological recovery in patients with mild traumatic brain injury (mTBI). ⋯ The median decrease in score was 4 for the atorvastatin group and 10.5 for the placebo group (χ2(1) = 0.8750; p = 0.3496). No serious adverse events occurred, and there was no significant difference in the incidence of adverse events in the two treatment groups. Atorvastatin administration for 7 days post-injury was safe, but there were no significant differences in neurological recovery post-mTBI with atorvastatin.
-
Journal of neurotrauma · Feb 2017
Traumatic brain injury in domestic violence victims: a retrospective study at the Barrow Neurological Institute.
Domestic violence is a national health crisis, which affects people of all ages, races, and socioeconomic classes. Traumatic brain injury is common in victims because of the high frequency of head and neck injuries inflicted through abuse. These recurrent injuries can lead to chronic symptoms with high morbidity. ⋯ Traumatic brain injury is a frequent sequela of domestic violence, from which many victims sustain multiple injuries without seeking medical care. Brain injuries are often sustained over many years and lead to lasting physical, behavioral, and cognitive consequences. Better understanding of these injuries will lead to improved care for this population.
-
Journal of neurotrauma · Feb 2017
ReviewReview: CNS Injury and NADPH Oxidase: Oxidative Stress and Therapeutic Targets.
Injury to the central nervous system (CNS) includes both traumatic brain and spinal cord injury (TBI and SCI, respectively). These injuries, which are heterogeneous and, therefore, difficult to treat, result in long-lasting functional, cognitive, and behavioral deficits. Severity of injury is determined by multiple factors, and is largely mediated by the activity of the CNS inflammatory system, including the primary CNS immune cells, microglia. ⋯ ROS play a central role in inflammation, contributing to cytokine translation and release, microglial polarization and activation, and clearance of damaged tissue. NOX has been suggested as a potential therapeutic target in CNS trauma, as inhibition of this enzyme family modulates inflammatory cell response and ROS production. The purpose of this review is to understand how the different NOX enzymes function and what role they play in the scope of CNS trauma.
-
Journal of neurotrauma · Feb 2017
Cerebrospinal fluid CCL2 is an early-response biomarker for blast overpressure wave- induced neurotrauma in rats.
Chemokines and their receptors are of great interest within the milieu of immune responses elicited in the central nervous system in response to trauma. Chemokine (C-C motif)) ligand 2 (CCL2), which is also known as monocyte chemotactic protein-1, has been implicated in the pathogenesis of traumatic brain injury (TBI), brain ischemia, Alzheimer's disease, and other neurodegenerative diseases. In this study, we investigated the time course of CCL2 accumulation in cerebrospinal fluid (CSF) after exposures to single and repeated blast overpressures of varied intensities along with the neuropathological changes and motor deficits resulting from these blast conditions. ⋯ CCL2 levels in CSF and plasma were tightly correlated with levels of CCL2 messenger RNA in cerebellum, the brain region most consistently neuropathologically disrupted by blast. In view of the roles of CCL2 that have been implicated in multiple neurodegenerative disorders, it is likely that the sustained high levels of CCL2 and the increased expression of its main receptor, CCR2, in the brain after blast may similarly contribute to neurodegenerative processes after blast exposure. In addition, the markedly elevated concentration of CCL2 in CSF might be a candidate early-response biomarker for diagnosis and prognosis of blast-induced TBI.
-
Journal of neurotrauma · Feb 2017
Glibenclamide attenuates blood-brain barrier disruption in adult mice following traumatic brain injury.
Glibenclamide is a hypoglycemic drug that is widely used for the treatment of diabetes mellitus type 2 (DM II), but it also plays a protective role following injury to the central nervous system (CNS). However, the precise mechanisms underlying its neuroprotective actions remain to be elucidated. Therefore, the present study evaluated the effects of glibenclamide on the blood-brain barrier (BBB) in a mouse model of traumatic brain injury (TBI). ⋯ Glibenclamide primarily attenuated apoptosis via the JNK/c-jun signaling pathway and resulted in an elevation of stretch injury-induced ZO-1 expression in bEnd.3 cells (p < 0.01). Glibenclamide downregulated the activity of the JNK/c-jun apoptosis-signaling pathway which, in turn, decreased apoptosis in endothelial cells (ECs). This may have prevented the disruption of the BBB in a mouse model of TBI.