Journal of neurotrauma
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Journal of neurotrauma · Jul 2007
Time window for voluntary exercise-induced increases in hippocampal neuroplasticity molecules after traumatic brain injury is severity dependent.
We recently found that an exercise-induced increase in hippocampal brain-derived neurotrophic factor (BDNF) is dependent when exercise is initiated after traumatic brain injury (TBI). When voluntary exercise was delayed by 2 weeks after a mild fluid-percussion injury (FPI) in rats, an increase in BDNF and an improvement in behavioral outcome were observed. This suggests that following FPI there is a therapeutic window for the implementation of voluntary exercise. ⋯ Whereas BDNF levels significantly increased with exercise in the mild FPI rats that were exercised from PID 14 to 20, the moderate FPI rats only showed significant increases in BDNF when exercised from PID 30 to 36. In addition, moderate FPI rats that were allowed to exercise from PID 30 to 36 also exhibited significant increases in synapsin I and CREB. These results indicate that the time window for exercise-induced increases in BDNF, synapsin I, and CREB is dependent on injury severity.
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The response of trauma systems in rural areas is uncertain since distances between injury scenes and trauma care are considerable. Timely arrival at definitive care is critical for persons with traumatic brain injury (TBI) since secondary damage can occur during the hours following injury. We evaluated how the implementation of a trauma system in a predominately rural state affected the triage of TBI patients and their risk for mortality. ⋯ Following implementation of the trauma system, patients treated in Level I or II facilities were older (p = 0.019), more often had multiple injuries (p = 0.0002), and had more severe TBI (p = 0.008). After controlling for confounders, transferred patients and those directly admitted were less likely to die in 72 h in the post-system than the pre-system (odds ratio [OR] = 0.56, 95% confidence interval (CI) = 0.36, 0.88; OR = 0.50, 95% CI = 0.32, 0.79). Implementation of the Iowa trauma system seems to have led to more appropriate triage and transport for TBI patients, and this likely contributed to reduced in-hospital mortality.
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Journal of neurotrauma · Jul 2007
Comparative StudyMulti-modal magnetic resonance imaging alterations in two rat models of mild neurotrauma.
Magnetic resonance imaging (MRI) is increasingly used in the assessment of the severity and progression of neurotrauma. We evaluated temporal and regional changes after mild fluid percussion (FPI) and controlled cortical impact (CCI) injury using T2-weighted-imaging (T2WI) and diffusion-weighted imaging (DWI) MRI over 7 days. Region of interest analysis of brain areas distant to the injury site (such as the hippocampus, retrosplenial and piriform cortices, and the thalamus) was undertaken. ⋯ Histological assessment of FPI animals revealed numerous shrunken cells in the hippocampus and thalamus, but other regions showed little damage. Increased immunohistochemical staining for microglia and astroglia at 7 days post-injury was greater in FPI animals within the affected brain regions. In summary, traumatic brain injury is less severe in mild CCI than FPI, based on the temporal events assessed with MRI.
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Journal of neurotrauma · Jul 2007
Statins increase neurogenesis in the dentate gyrus, reduce delayed neuronal death in the hippocampal CA3 region, and improve spatial learning in rat after traumatic brain injury.
Traumatic brain injury (TBI) remains a major public health problem globally. Presently, there is no way to restore cognitive deficits caused by TBI. In this study, we seek to evaluate the effect of statins (simvastatin and atorvastatin) on the spatial learning and neurogenesis in rats subjected to controlled cortical impact. ⋯ Brain tissue was processed for immunohistochemical staining to identify newly generated cells and vessels. Our data show that (1) treatment of TBI with statins improves spatial learning on days 31-35 after onset of TBI; (2) in the non-neurogenic region of the hippocampal CA3 region, statin treatment reduces the neuronal loss after TBI, demonstrating the neuroprotective effect of statins; (3) in the neurogenic region of the dentate gyrus, treatment of TBI with statins enhances neurogenesis; (4) statin treatment augments TBI-induced angiogenesis; and (5) treatment with simvastatin at the same dose provides a therapeutic effect superior to treatment with atorvastatin. These results suggest that statins may be candidates for treatment of TBI.
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Journal of neurotrauma · Jul 2007
The novel apolipoprotein E-based peptide COG1410 improves sensorimotor performance and reduces injury magnitude following cortical contusion injury.
It has previously been shown that small peptide molecules derived from the apolipoprotein E (ApoE) receptor binding region are anti-inflammatory in nature and can improve outcome following head injury. The present study evaluated the preclinical efficacy of COG1410, a small molecule ApoE-mimetic peptide (1410 daltons), following cortical contusion injury (CCI). Animals were prepared with a unilateral CCI of the sensorimotor cortex (SMC) or sham procedure. ⋯ The 0.8 mg/kg dose also reduced the number of glial fibrillary acid protein (GFAP+) reactive cells in the injured cortex. These results suggest that a single dose of COG1410 facilitates behavioral recovery and provides neuroprotection in a dose and task-dependent manner. Thus, the continued clinical development of ApoE based therapeutics is warranted and could represent a novel strategy for the treatment of traumatic brain injuries.