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Editorial Reviews. About the Author. Biography I majored in Science in from the University of Toronto. Physics and Chemistry were especially, my favourite.
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Notably, this model induces diffuse axonal injury DAI in the white matter with the identical appearance as found in human TBI. Additionally, atypical or disrupted NOR morphology was observed throughout the white matter, including in regions that did not display overt axonal damage identified as swollen axonal profiles. Finally, we also found increased numbers of void and amorphous nodes following injury.

Consequently, these data demonstrate sodium channel changes and global NOR pathology beyond regions of axonal pathology in mTBI. These changes may play a role in the brain network dysfunction that underlies the clinical symptoms of mTBI. This work was supported by the Paul G. Diagnosis, monitoring and outcome prediction are essential for translating novel TBI treatments from rodent to man. Our objective was to develop and validate immunoassays for quantitative assessment of novel Astrocyte Injury Defined, AID neurotrauma biomarkers useful for both animal models and TBI patients.

The best performing antibody pairs were then selected for mesoscale discovery platform MSD assay prototypes. Keywords: translation, serum, cerebrospinal fluid, controlled cortical impact, outcome, breakdown product. While some spontaneous functional plasticity does occur following cervical SCI, the extent is limited and diaphragm paresis persists.

Anatomical plasticity following injury and treatment was investigated using transynaptic tracing and immunohistochemistry. Pseudorabies virus PRV was used to retrogradely and transneuronally trace the spinal phrenic circuitry ipsilateral to injury and assess integration of premotor spinal interneurons with phrenic motoneurons. Functional plasticity and respiratory recovery following dAIHc training was assessed with terminal diaphragm electromyography dEMG.

Hypercapnia trained animals showed a greater density of serotonergic axons within the spinal cord, yet surprisingly an increased BDNF expression within the medulla, when compared with untreated and air control animals. It was also found that 2 weeks of dAIHc training resulted in a greater recruitment of interneurons into ipsilateral phrenic circuitry when compared to untreated and air controls. Diaphragm EMG of the dAIHc trained animals resulted in modest improvement of the ipsilateral and contralateral diaphragm inspiratory amplitude as well as response to respiratory challenge.

These results therefore suggest that dAIHc is able to promote plasticity within the phrenic network following cervical SCI. Differences emerged within the visual network between Veterans with blast exposure, regardless of symptom presentation, and unexposed controls. Overall, blast exposure was related to functional hypoconnectivity in this the left lateral visual network, regardless of whether or not Veterans reported having acute clinical symptoms of mild TBI. These findings suggest blast exposure may alter the connections between visual perception and emotional processing.

Additional research on the subconcussive effects of blast exposure is needed to further characterize this relationship. The majority of injured axons do not become transected by the biomechanical forces, but they undergo alterations and eventually succumb to fragmentation.

The discovery that the enzyme SARM1 is an instructive signal in the execution of Wallerian degeneration in simpler models of injury raises the question of whether the same molecular mechanism is encountered in TAI and, if so, whether interventions to block SARM1 can protect injured axons and improve TBI outcomes. Here we tested the role of SARM1 in TAI using the impact acceleration model and focusing on the corticospinal tract, a descending pathway responsible for skilled movements.

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Our findings indicate that SARM1 deletion or pharmacological inhibition preserve the structural and functional connectivity of the injured corticospinal tract and, by doing so, they preserve skilled motor function, pointing to the potential translational significance of this target in TBI. Prior research has established that bleed volume on CT is prognostically significant.

However, it is now recognized that the adverse effects, particularly of repetitive mTBI, continue for many years after the original event. Previously, we showed that chronic treatment with the drug Anatabine acutely after the injury improved cognitive functions and decreased inflammation.

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However, little is known about the benefits of the delayed administration of the same drug at chronic time points postinjury. The purpose of the current study is to test the extent to which a delayed treatment can be beneficial after mTBI.

We examined the effect of Anatabine treatment on the functional and anatomical recovery from mTBI. Delayed treatment with Anatabine for 3 months returned both the motor performance and spatial learning back to the sham levels. Pathological analysis of the brain tissue for inflammatory markers and tau are ongoing. Axonal regeneration in the central nervous system CNS is a high energy demanding process. Extrinsic insults and intrinsic restriction lead to injured CNS axons in a state of local energy crisis, thus raising a fundamental question as to whether recovering energy deficit facilitates CNS regeneration following injury.

Notably, regenerating CST axons are able to form functional synapses, transmit electrophysiological signals, and promote motor functional recovery. Importantly, our energy crisis model is further supported by the finding that systemic administration of creatine, a bioenergetic compound, significantly facilitates CST regeneration.

Thus, our study provides a new mechanistic insight into intrinsic regeneration failure in the CNS and suggests that enhancing local energy recovery is a promising strategy to promote axonal regeneration and functional recovery after CNS injuries. Traumatic brain injury TBI elicits immediate neuroinflammatory events that cause acute cognitive, motor, and behavioral disturbances. Despite resolution of acute complications, functional impairments can develop after TBI. To quantify cortical gene expression, Nanostring's Neuropathology gene expression assay genes was used.

Moreover, when microglia were eliminated, TBI caused robust increase in genes related to angiogenesis. Thus, microglia promote persistent neuropathological transcriptional and functional impairment after diffuse TBI. Microglial survival is dependent on the colony stimulating factor receptor 1 CSFR1.

CSFR1 inhibitors have been developed to investigate microglial function during physiological and pathophysiological conditions. Using the CSFR1 inhibitor, PLX, we set out to test the hypothesis that removal of neurotoxic microglia during the chronic stages of TBI will improve neurological recovery and reduce chronic neurodegeneration. At 12 WPI, mice were anesthetized, and brains were prepared for neuropathological assessments. A second cohort of animals were anesthetized at 8 WPI and brains were harvested for flow cytometry analysis.

Over 13 million people in the U. Our lab has demonstrated that 7. Stimulation occurred at 7. Therefore, the data suggests that even acute stimulation had beneficial effects on cognitive outcome and that, regardless of timing, stimulation resulted in persistent but not indefinite benefits.

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Furthermore, 30min of stimulation immediately preceding BM impaired performance. Our data continue to support the potential of 7. A comorbidity of TBI is the generation of neuropsychiatric disorders including depression and aberrant social behaviors. Wang 1,4. Pathophysiological mechanism of traumatic brain injury TBI is heterogeneous including axonal injury, white matter integrity, microvascular injury and neuroinflammation. In parallel, MRI scanning sequences were carried out at Serum GFAP signals peak at d1 across models. In contrast, mean diffusivity MD is high in WM at d2 and remains high in the lesion site.

Compared to microglia, astrocyte activation has been reported to occur in a more delayed fashion following brain trauma. Past studies have focused on the reparative processes driven by astrocyte activation such as glial scar formation and its role in limiting secondary injury. Recently, the duality of neurotoxic A1 vs. Tissue expression of cytokines and astrocyte activation markers was evaluated by qPCR. Conclusions: Juvenile FPI results in rapid astrocyte activation which contributes importantly to increased inflammatory cytokine expression. Ongoing studies will compare the relative contribution of astrocytes and microglia to inflammatory mediator production and elucidate how astrocyte activation changes over time.

Mitochondria are dynamic organelles continuously undergoing fusion and fission and their levels are regulated by the process of mitochondrial biogenesis MB and mitophagy. Activation of MB may be an important intervention to restore mitochondrial and brain function.

Books by Sheila Ber (Author of Arthritis Help and Advice)

Stoica 1 , Alan I. In the mouse brain, Hv1 is expressed by microglia but not neurons or astrocytes. However, neither the cellular mechanisms nor critical role of Hv1 in the pathophysiology of traumatic brain injury TBI are fully understood. Spinal cord injury SCI causes not only sensorimotor deficits, neuropathic pain, and autonomic dysfunction but also varying degrees of neuropsychological abnormalities.

Epidemiological studies report males have a higher likelihood of getting a SCI than females, however, little is known about the effect of biological sex on brain dysfunction and injury mechanisms. Using NanoString technology, about neuroinflammatory genes were analyzed in injured spinal cord and cerebral cortex. However, at 8 months after SCI, female mice revealed less neuroinflammation compared with male animals. Collectively, these findings indicate that sexual differences on functional outcome after SCI are associated with disrupted neuroinflammation not only in injured site but also in remote brain region.

Thus, biological sex should be considered when designing new therapeutic agents.

The Case Against Reality

Traumatic brain injury TBI is a risk factor for neurodegenerative disease, in particular chronic traumatic encephalopathy CTE. Current consensus criteria define the pathognomonic lesion of CTE as patchy tau pathology within neurons and astrocytes at the depths of cortical sulci. However, it remains unknown which aspect of this pathology might be unique to CTE.

Representative sections were stained for tau and maps of neuronal and astroglial pathologies generated to examine their respective cortical distributions. Comprehensive cell mapping revealed that astrocytes, but not neurofibrillary tangles NTFs , preferentially concentrate at depths of sulci. Here we show that astroglial tau pathologies in CTE are phenotypically and conformationally distinct from adjacent NFTs. These findings underscore the need for continued interrogation and refinement of our understanding of the pathology of CTE.

Methods: Our lab has developed an innovative strategy for neurologic injury assessment that combines nanofluidic technologies to isolate EVs from patient plasma with downstream analysis of EV protein or nucleic acid cargo in a platform we call exoTENPO.