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Modafinil for the Improvement of Patient Outcomes Following Traumatic Brain Injury
Conclusion. Modafinil is a central nervous system stimulant with well-established effectiveness in the treatment of narcolepsy and shift-work sleep disorder. There is conflicting evidence about the benefits of modafinil in the treatment of fatigue and EDS secondary to TBI. One randomized, controlled study states that modafinil does not significantly improve patient wakefulness, while another concludes that modafinil corrects EDS but not fatigue. An observational study provides evidence that modafinil increases alertness in fatigued patients with past medical history of brainstem diencephalic stroke or multiple sclerosis. ...
Source: Innovations in Clinical Neuroscience - April 1, 2018 Category: Neuroscience Authors: ICNS Online Editor Tags: Current Issue Review excessive daytime sleep fatigue head injury modafinil stroke TBI traumatic brain injury Source Type: research

Editor ’ s Message: September –October 2016 Issue Highlights
Dear Colleagues: Welcome to the September-October 2016 issue of Innovations in Clinical Neuroscience (ICNS). As the official journal of the CNS Summit, the International Society for CNS Drug Development (ISCDD), and the International Society for CNS Clinical Trials and Methodology (ISCTM), an important part of our editorial mission is to accelerate and enhance of the development of cheaper, more effective treatments for our patients through technology, collaboration, and innovation—not just in neuroscience but in all disciplines of medicine and among all involved entities, including clinicians, researchers, and members o...
Source: Innovations in Clinical Neuroscience - October 9, 2016 Category: Neuroscience Authors: ICN Online Editor Tags: Current Issue Drug Development Editor's Message: Issue Highlights Neurology Psychiatry Trial Methodology Amir H. Kalali CNS Summit Innovations in Clinical Neuroscience ISCDD ISCTM Source Type: research

Parecoxib Protects Mouse Cortical Neurons Against OGD/R Induced Neurotoxicity by Up-Regulating Bcl-2.
In this study, we found parecoxib could protect against neurotoxicity induced by 4 h oxygen-glucose deprivation (OGD) plus reoxgenation for 20 h, a widely used in vitro model of ischemia/reperfusion. In addition, we characterized the molecular mechanism of parecoxib's neuroprotection. We found parecoxib was able to activate CREB, and subsequently maintained the expression of Bcl-2, which is an important mitochondria-associated protein. Inhibition of endogenous Bcl-2 expression by transfection of Bcl-2-shRNA significantly attenuated the neuroprotective effects of parecoxib treatment. Furthermore, ATP production assay and ...
Source: Neurochemical Research - June 2, 2015 Category: Neuroscience Authors: Wang Y, Ma W, Jia A, Guo Q Tags: Neurochem Res Source Type: research