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Alaa Kamnaksh, Noora Puhakka, Idrish Ali, Gregory Smith, Roxanne Aniceto, Jesse McCullough, Shalini Das Gupta, Xavier Ekolle Ndode-Ekane, Rhys Brady, Pablo Casillas-Espinosa, Matt Hudson, Cesar Santana-Gomez, Riikka Immonen, Pedro Andrade de Abreu, Nigel Jones, Sandy Shultz, Richard J Staba, Terence J O'Brien, Denes Agoston, Asla Pitkänen
The Epilepsy Bioinformatics Study for Antiepileptogenic Therapy (EpiBioS4Rx) is an international, multicenter, multidisciplinary study aimed at preventing epileptogenesis (EpiBioS4Rx: One of the study's major objectives is the discovery of diagnostic, prognostic, and predictive plasma protein and microRNA (miRNA) biomarkers that are sensitive, specific, and translatable to the human condition. Epilepsy due to structural brain abnormalities, secondary to neurological insults such as traumatic brain injury (TBI), currently represents ∼50% of all epilepsy cases...
November 26, 2018: Epilepsy Research
Pedro Andrade, Ivette Banuelos-Cabrera, Niina Lapinlampi, Tomi Paananen, Robert Ciszek, Xavier Ekolle Ndode-Ekane, Asla Pitkanen
Severe traumatic brain injury (TBI) induces seizures or status epilepticus (SE) in 20%-30% of patients during the acute phase. We hypothesized that severe TBI induced with lateral fluid-percussion injury (FPI) triggers post-impact SE. Adult Sprague-Dawley male rats were anesthetized with isoflurane and randomized into sham-operated experimental control or lateral FPI-induced severe TBI groups. Electrodes were implanted right after impact or sham-operation, then video-electroencephalogram (EGG) monitoring was started...
December 13, 2018: Journal of Neurotrauma
Abdurrahman Çetin, Engin Deveci
This study aimed to investigate the antioxidative and anti-inflammatory effects of caffeic acid phenethyl ester (CAPE) on damage caused to cerebellum tissue by diffuse traumatic head trauma via biochemical, histopathologic, and immuno-histochemical methods. Male Sprague-Dawley (300-350g) rats were subjected to traumatic brain injury with a weight-drop device (300 g-1 m weight-height impact). Twenty-four adult rats were randomly divided into three equal groups of 8, including a control group, traumatic brain injury (TBI) group, and TBI+CAPE treatment group (10μmol/kg/i...
December 13, 2018: Folia Morphologica (Warsz)
Mohammad Ali Mirshekar, Alireza Sarkaki, Yaghoub Farbood, Mohammad Kazem Gharib Naseri, Mohammad Badavi, Mohammad Taghi Mansouri, Abbas Haghparast
Objectives: Traumatic brain injury (TBI) is one of the main causes of intellectual and cognitive disabilities. Clinically, it is essential to limit the development of cognitive impairment after TBI. In the present study, the neuroprotective effects of gallic acid (GA) on neurological score, memory, long-term potentiation (LTP) from hippocampal dentate gyrus (hDG), brain lipid peroxidation and cytokines after TBI were evaluated. Materials and Methods: Seventy-two adult male Wistar rats divided randomly into three groups with 24 in each: Veh + Sham, Veh + TBI and GA + TBI (GA; 100 mg/kg, PO for 7 days before TBI induction)...
October 2018: Iranian Journal of Basic Medical Sciences
Hong-Mei Zhang, Wei Chen, Rui-Ning Liu, Yan Zhao
Introduction: Secondary brain injury is a major factor that affects the prognosis and outcome of traumatic brain injury (TBI) patients. Secondary brain edema is considered to be an initiating factor in secondary brain injury after TBI. A previous study has indicated that Notch signaling activation contributes to neuron death in mice affected by stroke; however, its role in neuronal oxidation stress for brain edema after TBI is not well established. Apparent diffusion coefficient (ADC) values can represent the brain edema after TBI...
2018: Drug Design, Development and Therapy
Yanlu Zhang, Michael Chopp, Zheng Gang Zhang, Yi Zhang, Li Zhang, Mei Lu, Talan Zhang, Stefan Winter, Edith Doppler, Hemma Brandstäetter, Asim Mahmood, Ye Xiong
BACKGROUND: Cerebrolysin is a neuropeptide preparation with neuroprotective and neurotrophic properties. Our previous study demonstrates that cerebrolysin significantly improves functional recovery in rats after mild traumatic brain injury (mTBI). OBJECTIVE: To determine histological outcomes associated with therapeutic effects of cerebrolysin on functional recovery after TBI. METHODS: In this prospective, randomized, blinded, and placebo-controlled study, adult Wistar rats with mild TBI induced by a closed head impact were randomly assigned to one of the cerebrolysin dose groups (0...
November 30, 2018: Neurorehabilitation and Neural Repair
Sindhu K Madathil, Bernard S Wilfred, Sarah E Urankar, Weihong Yang, Lai Yee Leung, Janice S Gilsdorf, Deborah A Shear
Microglial activation is a pathological hallmark of traumatic brain injury (TBI). Following brain injury, activated microglia/macrophages adopt different phenotypes, generally categorized as M-1, or classically activated, and M-2, or alternatively activated. While the M-1, or pro-inflammatory phenotype is detrimental to recovery, M-2, or the anti-inflammatory phenotype, aids in brain repair. Recent findings also suggest the existence of mixed phenotype following brain injury, where activated microglia simultaneously express both M-1 and M-2 markers...
2018: Frontiers in Neurology
Lital Magid, Sami Heymann, Merav Elgali, Liat Avram, Yoram Cohen, Sigal Liraz-Zaltsman, Raphael Mechoulam, Esther Shohami
Cannabis is one of the most widely used plant drugs in the world today. In spite of the large number of scientific reports on medical marijuana there still exists much controversy surrounding its use and the potential for abuse due to the undesirable psychotropic effects. However, recent developments in medicinal chemistry of novel non-psychoactive synthetic cannabinoids have indicated that it is possible to separate some of the therapeutic effects from the psychoactivity. We have previously shown that treatment with the endocannabinoid 2-AG that binds to both CB1 and CB2 receptors 1 hr after traumatic brain injury in mice attenuates neurological deficits, edema formation, infarct volume, blood-brain barrier permeability, neuronal cell loss at the CA3 hippocampal region and neuroinflammation...
November 29, 2018: Journal of Neurotrauma
Li-Hua Chen, Hong-Tian Zhang, Ru-Xiang Xu, Wen-De Li, Hao Zhao, Yi Yang, Kai Sun
Objectives: methyl-D-aspartate NMDA receptor (NMDAR) and aquaporin 4 (AQP4) are involved in the molecular cascade of edema after traumatic brain injury (TBI) and are potential targets of studies in pharmacology and medicine. However, their association and interactions are still unknown. Materials and Methods: We established a rat TBI model in this study. The cellular distribution patterns of AQP4 after inhibition of NMDAR were determined by Western blotting and immunoreactive staining...
November 2018: Iranian Journal of Basic Medical Sciences
Chellappan Praveen Rajneesh, Chien-Hung Lai, Shih-Ching Chen, Tsung-Hsun Hsieh, Hung-Yen Chin, Chih-Wei Peng
OBJECTIVE: Traumatic brain injury (TBI) is a global scenario with high mortality and disability, which does not have an effectual and approved therapy till now. Bladder dysfunction is a major symptom after TBI, and this study deals with the alleviation of bladder function in TBI rats, with the aid of deep brain stimulations (DBS). METHODS: TBI was induced by weight drop model (WDM) and standardized with the experimental subjects with variable heights for weight dropping...
November 24, 2018: International Urology and Nephrology
Adaora A Okigbo, Michael S Helkowski, Brittany J Royes, Isabel H Bleimeister, Tracey R Lam, Gina C Bao, Jeffrey P Cheng, Corina O Bondi, Anthony E Kline
Numerous pharmacotherapies have been evaluated after experimental traumatic brain injury (TBI). While amantadine (AMT) has shown potential for clinical efficacy, the few studies on its effectiveness have been mixed. It is possible that suboptimal dosing, due to the evaluation of only one dose, may be causing the discrepancies in outcomes. Hence, the goal of the current study was to conduct a dose response of AMT after TBI to determine an optimal behavioral benefit. Anesthetized adult male rats received either a cortical impact of moderate severity or sham injury and then were randomly assigned to receive once daily intraperitoneally injections of AMT (10, 20, or 40 mg/kg) or saline vehicle (VEH, 1 mL/kg) commencing 24 h after injury for 19 days...
November 22, 2018: Neuroscience Letters
Askin Esen Hasturk, Emre Cemal Gokce, Erdal Resit Yilmaz, Bahriye Horasanli, Oya Evirgen, Nazli Hayirli, Hilal Gokturk, Imge Erguder, Belgin Can
Purpose: The aim of the present study was to investigate the effect of etanercept (ETA) on histopathological and biochemical changes after traumatic brain injury (TBI) in rats. Materials and Methods: Thirty-six male Wistar albino rats were distributed into three groups ( n = 12 each). Control group rats were not subjected to trauma. Trauma group rats were subjected to TBI only. ETA group rats were subjected to TBI plus ETA (5 mg/kg intraperitoneal [i.p.]). The groups were further subdivided into those sacrificed in the hyperacute stage (1 h after TBI) (control-1, trauma-1, and ETA-1 groups) and the acute stage (6 h after TBI) (control-6, trauma-6, and ETA-6 groups)...
October 2018: Asian Journal of Neurosurgery
Gina Bao, Isabel Bleimeister, Lydia Zimmerman, JoDy Wellcome, Peter Niesman, Hannah Radabaugh, Corina O Bondi, Anthony E Kline
The administration of haloperidol (HAL) once daily for 19 days after experimental traumatic brain injury (TBI) impedes recovery and attenuates the efficacy of environmental enrichment (EE). However, it is unknown how intermittent administration of HAL affects the recovery process when paired with EE. Addressing the uncertainty is relevant because daily HAL is not always warranted to manage TBI-induced agitation in the clinic, and indeed intermittent therapy may be a more common approach. Hence, the aim of the study was to test the hypothesis that intermittent HAL would neither impair recovery in standard (STD)-housed controls nor attenuate the efficacy of EE...
November 20, 2018: Journal of Neurotrauma
Natalie N Nawarawong, Megan Slaker, Matt Muelbl, Alok S Shah, Rachel Chiariello, Lindsay D Nelson, Matthew D Budde, Brian D Stemper, Christopher M Olsen
Each year, traumatic brain injuries (TBI) affect millions worldwide. Mild TBIs (mTBI) are the most prevalent and can lead to a range of neurobehavioral problems, including substance abuse. A single blast exposure, inducing mTBI alters the medial prefrontal cortex, an area implicated in addiction, for at least 30 days post injury in rats. Repeated blast exposures result in greater physiological and behavioral dysfunction than single exposure, however, the impact of repeated mTBI on addiction is unknown. In this study, the effect of mTBI on various stages of oxycodone use was examined...
November 20, 2018: European Journal of Neuroscience
Saman Sargolzaei, Yan Cai, Melissa J Walker, David A Hovda, Neil G Harris, Christopher C Giza
Experimental models have been proven to be valuable tools to understand downstream cellular mechanisms of Traumatic Brain Injury (TBI). The models allow for reduction of confounding variables and tighter control of varying parameters. It has been recently reported that craniectomy induces pro-inflammatory responses, which therefore needs to be properly addressed given the fact that craniectomy is often considered a control procedure for experimental TBI models. The current study aims to determine whether a craniectomy induces alterations in Resting State Network (RSN) in a developmental rodent model...
July 2018: Conference Proceedings: Annual International Conference of the IEEE Engineering in Medicine and Biology Society
Fei Niu, Jinqian Dong, Xiaojian Xu, Bin Zhang, Baiyun Liu
BACKGROUND: Growing evidences have implicated dysfunctional mitochondria in the pathophysiology of neurodegenerative disorders. Selective degradation of dysfunctional mitochondria is termed mitophagy and constitutes a pivotal component of mitochondrial quality control to maintain cellular homeostasis. Mitochondrial fission plays prominent roles in controlling mitochondrial shape and function. However, it is unclear whether mitochondrial fission in the context of eliminating damaged mitochondria is involved in traumatic brain injury (TBI)...
November 12, 2018: World Neurosurgery
Liang Wu, Ning-Ning Ji, Hang Wang, Jing-Yu Hua, Guo-Lin Sun, Pan-Pan Chen, Rong Hua, Yong-Mei Zhang
The effects of local factors on the activation of immune cells infiltrating the CNS in rat model of traumatic brain injury (TBI) remains to be defined. The cytokine IL-15 is crucial in the development and activation of CD8 T lymphocytes, a prominent lymphocytic population identified in TBI lesions. We investigated whether IL-15 originates from astrocytes as well as evoke the CD8 T lymphocyte response in TBI. We observed that astrocytes were activated in TBI rat model, with IL-15 overexpressed on the astrocytic surface...
November 15, 2018: Journal of Neurotrauma
Jyothsna Chitturi, Vijayalakshmi Santhakumar, Sridhar Kannurpatti
Oxidative energy metabolism is depressed after mild/moderate TBI during early development, accompanied by behavioral debilitation and secondary neuronal death. TBI metabolome analysis revealed broad effects with a striking impact on energy metabolism. Our studies on mitochondrial modulators and their effects on brain function have shown that Kaempferol, a stimulator of the mitochondrial Ca2+ uniporter channel (mCU), enhanced neural and neurovascular activity in the normal and improved stimulus-induced brain activation and behavior after TBI during early development...
November 15, 2018: Journal of Neurotrauma
Shiping Li, Qiaoying Zhang, Peiwu Li
Background: This study evaluated the protective effects of epifriedelinol (EFD) in a rat model of traumatic brain injury (TBI). Methodology: TBI was induced by dropping a weight from a specific height. The animals were separated into control, TBI, and EFD 100 and 200 mg/kg groups. The latter received 100 and 200 mg/kg EFD, respectively, for 2 days beginning 30 min after inducing TBI. The neurological examination score, permeability of the blood-brain barrier (BBB), water content of the brain, cytokine levels, and oxidative stress parameters were measured in the rats...
2018: Translational Neuroscience
Xiangrong Chen, Zhigang Pan, Zhongning Fang, Weibin Lin, Shukai Wu, Fuxing Yang, Yasong Li, Huangde Fu, Hongzhi Gao, Shun Li
BACKGROUND: Enhancing autophagy after traumatic brain injury (TBI) may decrease the expression of neuronal apoptosis-related molecules. Autophagy-mediated neuronal survival is regulated by the sirtuin family of proteins (SIRT). Omega-3 polyunsaturated fatty acids (ω-3 PUFA) are known to have antioxidative and anti-inflammatory effects. We previously demonstrated that ω-3 PUFA supplementation attenuated neuronal apoptosis by modulating the neuroinflammatory response through SIRT1-mediated deacetylation of the HMGB1/NF-κB pathway, leading to neuroprotective effects following experimental traumatic brain injury (TBI)...
November 8, 2018: Journal of Neuroinflammation
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