scholarly journals The Role of BDNF in Experimental and Clinical Traumatic Brain Injury

2021 ◽  
Vol 22 (7) ◽  
pp. 3582
Author(s):  
David Gustafsson ◽  
Andrea Klang ◽  
Sebastian Thams ◽  
Elham Rostami

Traumatic brain injury is one of the leading causes of mortality and morbidity in the world with no current pharmacological treatment. The role of BDNF in neural repair and regeneration is well established and has also been the focus of TBI research. Here, we review experimental animal models assessing BDNF expression following injury as well as clinical studies in humans including the role of BDNF polymorphism in TBI. There is a large heterogeneity in experimental setups and hence the results with different regional and temporal changes in BDNF expression. Several studies have also assessed different interventions to affect the BDNF expression following injury. Clinical studies highlight the importance of BDNF polymorphism in the outcome and indicate a protective role of BDNF polymorphism following injury. Considering the possibility of affecting the BDNF pathway with available substances, we discuss future studies using transgenic mice as well as iPSC in order to understand the underlying mechanism of BDNF polymorphism in TBI and develop a possible pharmacological treatment.

2021 ◽  
Vol 28 ◽  
Author(s):  
Lucas Alexandre Santos Marzano ◽  
Fabyolla Lúcia Macedo de Castro ◽  
Caroline Amaral Machado ◽  
João Luís Vieira Monteiro de Barros ◽  
Thiago Macedo e Cordeiro ◽  
...  

: Traumatic brain injury (TBI) is a serious cause of disability and death among young and adult individuals, displaying complex pathophysiology including cellular and molecular mechanisms that are not fully elucidated. Many experimental and clinical studies investigated the potential relationship between TBI and the process by which neurons are formed in the brain, known as neurogenesis. Currently, there are no available treatments for TBI’s long-term consequences being the search for novel therapeutic targets, a goal of highest scientific and clinical priority. Some studies evaluated the benefits of treatments aimed at improving neurogenesis in TBI. In this scenario, herein, we reviewed current pre-clinical studies that evaluated different approaches to improving neurogenesis after TBI while achieving better cognitive outcomes, which may consist in interesting approaches for future treatments.


2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Xiaohong Li ◽  
Chong Chen ◽  
Xiping Yang ◽  
Jingjing Wang ◽  
Ming-liang Zhao ◽  
...  

How to promote neural repair following traumatic brain injury (TBI) has long been an intractable problem. Although acupuncture has been demonstrated to facilitate the neurological recovery, the underlying mechanism is elusive. Brain-derived neurotrophic factor (BDNF) exerts substantial protective effects for neurological disorders. In this study, we found that the level of BDNF and tropomyosin receptor kinase B (TrkB) was elevated spontaneously after TBI and reached up to the peak at 12 h. Nevertheless, this enhancement is quickly declined to the normal at 48 h. After combined stimulation at the acupoints of Baihui, Renzhong, Hegu, and Zusanli, we found that BDNF and TrkB were still significantly elevated at 168 h. We also observed that the downstream molecular p-Akt and p-Erk1/2 were significantly increased, suggesting that acupuncture could persistently activate the BDNF/TrkB pathway. To further verify that acupuncture improved recovery through activating BDNF/TrkB pathway, K252a (specific inhibitor of TrkB) was treated by injection stereotaxically into lateral ventricle. We observed that K252a could significantly prevent the acupuncture-induced amelioration of motor, sensation, cognition, and synaptic plasticity. These data indicated that acupuncture promoted the recovery of neurological impairment after TBI by activating BDNF/TrkB signaling pathway, providing new molecular mechanism for understanding traditional therapy of acupuncture.


Author(s):  
Farshid Rahimibashar ◽  
Masoum Khosh Fetrat ◽  
Keivan Gohari-Moghadam ◽  
Tannaz Jamialahmadi ◽  
Amirhossein Sahebkar

2016 ◽  
Vol 130 (4) ◽  
pp. 221-238 ◽  
Author(s):  
Abdelrahman Y. Fouda ◽  
Sandeep Artham ◽  
Azza B. El-Remessy ◽  
Susan C. Fagan

This review examines the published literature on the role of the renin-angiotensin system in neurovascular disorders including stroke, retinopathy, traumatic brain injury and cognitive impairment. The review presents both experimental and clinical studies conducted in the field, and sheds light on the translational gap and clinical underutilization of renin-angiotensin system modulators in neurovascular disorders.


Author(s):  
NIKOLAOS ANDREAS CHRYSANTHAKOPOULOS ◽  
PANAGIOTIS ANDREAS CHRYSANTHAKOPOULOS

Gliomas are the most common primary and aggressive intracranial tumors, represent 80% of malignant brain tumors, and despite the fact that are relatively rare tumors are responsible for significant mortality and morbidity. Glioblastoma multiforme (GBM) or diffuse astrocytoma, WHO grade IV, is the most common and aggressive primary central nervous system malignancy, represents 45% of all gliomas, shows an average incidence of 3.19/100,000 individuals, its median age of diagnosis is 64 years, and the median survival is 15 months as the 5-year relative survival is 5%. Previous studies have investigated the possible role of genetic and environmental factors in GBM pathogenesis; however, the majority of GBM cases were sporadic and certain risk factors have not been detected. GBM is divided into primary and secondary subtypes which develop through different genetic pathways, affect patients at different ages, and have differences in clinical outcomes, as show a great morphological and genetic heterogeneity. The role of traumatic brain injury (TBI) in GBM formation has been investigated in many previous reports which have hypothesized that TBI may predispose to gliomagenesis; however, the outcomes were highly controversial. Some of those researches have proposed a supposed pathogenesis model that involves a post-traumatic inflammation, stem and progenitor cell transformation, and gliomagenesis. Other similar studies have involved transcription factors associated with TBI such as p53, hypoxia-inducible factor-1a (HIF-1a), and c-Myc. On the other hand, the possibility of a pre-existing tumor rather than a trauma-induced tumor is very possible in such cases.


2020 ◽  
Vol 11 (2) ◽  
pp. 137-144 ◽  
Author(s):  
Tahereh Farkhondeh ◽  
Saeed Samarghandian ◽  
Babak Roshanravan ◽  
Leila Peivasteh-roudsari

Traumatic Brain Injury (TBI) is one of the main causes of mortality and morbidity worldwide with no suitable treatment. The present study was designed to review the present literature about the protective effects of curcumin and the underlying mechanism against TBI. All published English language papers from beginning to 2019 were selected in this study. The findings indicate that curcumin may be effective against TBI outcomes by modulating the molecular signaling pathways involved in oxidative stress, inflammation, apoptosis, and autophagy. However, more experimental studies should be done to identify all mechanisms involved in the pathogenesis of TBI. Patents for Curcumin and chronic inflammation and traumatic brain injury management (WO2017097805A1 and US9101580B2) were published. In conclusion, the present study confirmed the potential therapeutic impact of curcumin for treating TBI.


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