Recovery of corticospinal tract injured by traumatic axonal injury at the subcortical white matter:a case report

The corticospinal tract （CST） is a major neural tract for mo- tor function in the human brain. In addition, CST is mainly concerned with execution of movement of the hand （Jang, 2014）. However, few studies are reported on the mecha- nism underlying CST recovery after traumatic brain injury （Seo and Jang, 2015）. In this study, we report on a case that showed recovery of an injured CST by traumatic axonal injury （TAI） at subcortical white matter, as detected on fol- low-up diffusion tensor tractography （DTT）.

Animal model of repetitive mild traumatic brain injury for human traumatic axonal injury and chronic traumatic encephalopathy

Chronic traumatic encephalopathy（CTE）is a chronic neurodegenerative disease featured with tauopathy.CTE is tightly related with repetitive mild traumatic brain injury（m TBI）,which is interchangeably known as concussion（Mc Kee et al.,2009,2013）.This disease is differentiated by neuropathological features from other neurological diseases that involve tau protein aggregation and tangle formation abnormalities like Alzheimer＇s disease （AD）, frontotemporal dementia, and Parkinson- ism linked to chromosome 17 （FTDP-17）.

The occurrence of diffuse axonal injury in the brain:associated with the accumulation and clearance of myelin debris

The accumulation of myelin debris may be a major contributor to the inlfammatory response after diffuse axonal injury. In this study, we examined the accumulation and clearance of myelin debris in a rat model of diffuse axonal injury. Oil Red O staining was performed on sections from the cerebral cortex, hippocampus and brain stem to identify the myelin debris. Seven days after diffuse axonal injury, many Oil Red O-stained particles were observed in the cerebral cortex, hippocampus and brain stem. In the cerebral cortex and hippocampus, the amount of myelin debris peaked at 14 days after injury, and decreased signiifcantly at 28 days. In the brain stem, the amount of myelin debris peaked at 7 days after injury, and decreased signiifcantly at 14 and 28 days. In the cortex and hippocampus, some myelin debris could still be observed at 28 days after diffuse axonal injury. Our ifndings suggest that myelin debris may persist in the rat central ner-vous system after diffuse axonal injury, which would hinder recovery.

A novel technique using hydrophilic polymers to promote axonal fusion

The management of traumatic peripheral nerve injury remains a considerable concern for clinicians.With minimal innovations in surgical technique and a limited number of specialists trained to treat peripheral nerve injury,outcomes of surgical intervention have been unpredictable.The inability to manipulate the pathophysiology of nerve injury（i.e.,Wallerian degeneration） has left scientists and clinicians depending on the slow and lengthy process of axonal regeneration（-1 mm/day）.When axons are severed,the endings undergo calcium-mediated plasmalemmal sealing,which limits the ability of the axon to be primarily repaired.Polythethylene glycol（PEG） in combination with a bioengineered process overcomes the inability to fuse axons.The mechanism for PEG axonal fusion is not clearly understood,but multiple studies have shown that a providing a calcium-free environment is essential to the process known as PEG fusion.The proposed mechanism is PEG-induced lipid bilayer fusion by removing the hydration barrier surrounding the axolemma and reducing the activation energy required for membrane fusion to occur.This review highlights PEG fusion,its past and current studies,and future directions in PEG fusion.

Magnetic resonance imaging and cell-based neurorestorative therapy after brain injury

Restorative cell-based therapies for experimental brain injury, such as stroke and traumatic brain injury,substantially improve functional outcome. We discuss and review state of the art magnetic resonance imaging methodologies and their applications related to cell-based treatment after brain injury. We focus on the potential of magnetic resonance imaging technique and its associated challenges to obtain useful new information related to cell migration, distribution, and quantitation, as well as vascular and neuronal remodeling in response to cell-based therapy after brain injury. The noninvasive nature of imaging might more readily help with translation of cell-based therapy from the laboratory to the clinic.