scholarly journals Neuroprotection ofAlpinia katsumadaiSeed Extract against Neuronal Damage in the Ischemic Gerbil Hippocampus is Linked to Altered Brain-Derived Neurotrophic Factor

2011 ◽  
Vol 27 (1) ◽  
pp. 67 ◽  
Author(s):  
Hua Li ◽  
Joon Ha Park ◽  
Bingchun Yan ◽  
Ki-Yeon Yoo ◽  
Choong Hyun Lee ◽  
...  
Keyword(s):  
Neurotrophic Factor ◽  
Neuronal Damage ◽  
Brain Derived Neurotrophic Factor

scholarly journals Localized delivery of fibroblast growth factor–2 and brain-derived neurotrophic factor reduces spontaneous seizures in an epilepsy model

2009 ◽  
Vol 106 (17) ◽  
pp. 7191-7196 ◽  
Author(s):  
Beatrice Paradiso ◽  
Peggy Marconi ◽  
Silvia Zucchini ◽  
Elena Berto ◽  
Anna Binaschi ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Neurotrophic Factor ◽  
Viral Vectors ◽  
Neuronal Damage ◽  
Brain Derived Neurotrophic Factor ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Damage Limitation

A loss of neurons is observed in the hippocampus of many patients with epilepsies of temporal lobe origin. It has been hypothesized that damage limitation or repair, for example using neurotrophic factors (NTFs), may prevent the transformation of a normal tissue into epileptic (epileptogenesis). Here, we used viral vectors to locally supplement two NTFs, fibroblast growth factor–2 (FGF-2) and brain-derived neurotrophic factor (BDNF), when epileptogenic damage was already in place. These vectors were first characterized in vitro, where they increased proliferation of neural progenitors and favored their differentiation into neurons, and they were then tested in a model of status epilepticus-induced neurodegeneration and epileptogenesis. When injected in a lesioned hippocampus, FGF-2/BDNF expressing vectors increased neuronogenesis, embanked neuronal damage, and reduced epileptogenesis. It is concluded that reduction of damage reduces epileptogenesis and that supplementing specific NTFs in lesion areas represents a new approach to the therapy of neuronal damage and of its consequences.

Circulating Brain-Derived Neurotrophic Factor as a potential biomarker in stroke: a Systematic review and Meta-analysis

2021 ◽  
Author(s):  
Helia Mojtabavi ◽  
Zoha Shaka ◽  
Sara Momtazmanesh ◽  
Atra Ajdari ◽  
Nima Rezaei
Keyword(s):  
Physical Training ◽  
Neurotrophic Factor ◽  
Neuronal Damage ◽  
Meta Analysis ◽  
Brain Derived Neurotrophic Factor ◽  
Blood Levels ◽  
Cerebrovascular Event ◽  
Medical Databases ◽  
Potential Biomarker ◽  
Significant Difference

Abstract Background Stroke, an acute cerebrovascular event, is a leading cause of disability, placing a significant psycho-socioeconomic burden worldwide. Neuroplasticity is adaptation and reorganization following neuronal damage. Brain-derived neurotrophic factor (BDNF) is a neurotrophin coordinating neuroplasticity after various neurological disorders such as stroke. Methods We conducted a systematic search in the main electronic medical databases through January 2021 and identified studies that measured blood levels of BDNF in patients with stroke. The primary aim was to compare BDNF levels between patients with stroke and healthy controls (HC). The secondary aims included investigation of (1) longitudinal changes in the BDNF levels post-stroke, (2) effects of physical training, (3) repeated transcranial magnetic stimulation (rTMS), and presence of depression on BDNF levels in patients with stroke. Results Among 6243 reviewed records from PubMed, Web of Science, and Scopus, 62 studies were eligible for inclusion. Subjects with stroke, n = 1856, showed lower BDNF levels compared to HC, n=1191 (SMD [95%CI] = -1.04 [-1.49 to -0.58]). No significant difference was detected in the level of BDNF through time points past stroke. BDNF levels were lower in the patients with depression compared to non-depressed subjects (SMD [95%CI] = -0.60 [-1.10 to -0.10]). Physical training had an immediate positive effect on the BDNF levels and not statistically significant effect in the long term; SMD [95%CI] = 0.49 [0.09 to 0.88]) and SMD [95%CI] = 0.02 [-0.43 to 0.47]). Lastly, rTMS showed no effect on the level of BDNF with 0.00 SMD. Conclusions This study confirms that stroke significantly affects the level of BDNF in various domains such as cognition, affect, and motor function. We believe that BDNF could be regarded as a valuable diagnostic biomarker for acute stroke and a potential prognostic biomarker for depression and cognitive deficits.

Hypothermic Reperfusion after Cardiac Arrest Augments Brain-Derived Neurotrophic Factor Activation

2002 ◽  
Vol 22 (7) ◽  
pp. 843-851 ◽  
Author(s):  
Brian J. D'Cruz ◽  
Kristofer C. Fertig ◽  
Anthony J. Filiano ◽  
Shawn D. Hicks ◽  
Donald B. DeFranco ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Neurotrophic Factor ◽  
Mild Hypothermia ◽  
Neuronal Damage ◽  
Brain Derived Neurotrophic Factor ◽  
Global Cerebral Ischemia ◽  
Ischemia And Reperfusion ◽  
Bdnf Signaling ◽  
The Many ◽  
Asphyxial Cardiac Arrest

Induction of mild hypothermia improves neurologic outcome after global cerebral ischemia. This study measured levels of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in hippocampal tissue of rats after resuscitation from 8 minutes of normothermic, asphyxial cardiac arrest. After resuscitation, rats were maintained either at normal temperature (37°C) or cooled to mild hypothermia (33°C, beginning 60 minutes after resuscitation). After 12 or 24 hours, neurotrophin levels in hippocampus were measured by immunoblotting. Ischemia and reperfusion increased hippocampal levels of BDNF. Induction of hypothermia during reperfusion potentiated the increase in BDNF after 24 hours, but not after 12 hours. Levels of NGF were not increased by postresuscitation hypothermia. Hypothermia also increased tissue levels and tyrosine phosphorylation of TrkB, the receptor for BDNF. Increased BDNF levels were correlated with activation of the extracellularly regulated kinase (ERK), a downstream element in the signal transduction cascade induced by BDNF. In contrast to the many deleterious processes during ischemia and reperfusion that are inhibited by induced hypothermia, increasing BDNF levels is a potentially restorative process that is augmented. Increased activation of BDNF signaling is a possible mechanism by which mild hypothermia is able to reduce the neuronal damage typically occurring after cardiac arrest.

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