scholarly journals Chronic Antidepressants Potentiate via Sigma-1 Receptors the Brain-derived Neurotrophic Factor-induced Signaling for Glutamate Release

2006 ◽  
Vol 281 (18) ◽  
pp. 12941-12949 ◽  
Author(s):  
Yuki Yagasaki ◽  
Tadahiro Numakawa ◽  
Emi Kumamaru ◽  
Teruo Hayashi ◽  
Tsung-Ping Su ◽  
...  
Keyword(s):  
Neurotrophic Factor ◽  
Glutamate Release ◽  
Brain Derived Neurotrophic Factor ◽  
Sigma 1 ◽  
The Brain

scholarly journals Changes in the Brain-Derived Neurotrophic Factor Are Associated with Improvements in Diabetes Risk Factors after Exercise Training in Adolescents with Obesity: The HEARTY Randomized Controlled Trial

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Jeremy J. Walsh ◽  
Amedeo D’Angiulli ◽  
Jameason D. Cameron ◽  
Ronald J. Sigal ◽  
Glen P. Kenny ◽  
...  
Keyword(s):  
Risk Factors ◽  
Exercise Training ◽  
Neurotrophic Factor ◽  
Fasting Glucose ◽  
Brain Derived Neurotrophic Factor ◽  
Diabetes Risk ◽  
Model Assessment ◽  
Neurocognitive Deficits ◽  
Diabetes Risk Factors ◽  
The Brain

Obesity in youth increases the risk of type 2 diabetes (T2D), and both are risk factors for neurocognitive deficits. Exercise attenuates the risk of obesity and T2D while improving cognitive function. In adults, these benefits are associated with the actions of the brain-derived neurotrophic factor (BDNF), a protein critical in modulating neuroplasticity, glucose regulation, fat oxidation, and appetite regulation in adults. However, little research exists in youth. This study examined the associations between changes in diabetes risk factors and changes in BDNF levels after 6 months of exercise training in adolescents with obesity. The sample consisted of 202 postpubertal adolescents with obesity (70% females) aged 14–18 years who were randomized to 6 months of aerobic and/or resistance training or nonexercise control. All participants received a healthy eating plan designed to induce a 250/kcal deficit per day. Resting serum BDNF levels and diabetes risk factors, such as fasting glucose, insulin, homeostasis model assessment (HOMA-B—beta cell insulin secretory capacity) and (HOMA-IS—insulin sensitivity), and hemoglobin A1c (HbA1c), were measured after an overnight fast at baseline and 6 months. There were no significant intergroup differences on changes in BDNF or diabetes risk factors. In the exercise group, increases in BDNF were associated with reductions in fasting glucose (β = −6.57, SE = 3.37, p=0.05) and increases in HOMA-B (β = 0.093, SE = 0.03, p=0.004) after controlling for confounders. No associations were found between changes in diabetes risk factors and BDNF in controls. In conclusion, exercise-induced reductions in some diabetes risk factors were associated with increases in BDNF in adolescents with obesity, suggesting that exercise training may be an effective strategy to promote metabolic health and increases in BDNF, a protein favoring neuroplasticity. This trial is registered with ClinicalTrials.gov NCT00195858, September 12, 2005 (funded by the Canadian Institutes of Health Research).

Antiapoptotic activity maintenance of Brain Derived Neurotrophic Factor and the C fragment of the tetanus toxin genetic fusion protein

2008 ◽  
Vol 3 (2) ◽  
pp. 105-112 ◽  
Author(s):  
Jesús Ciriza ◽  
Marcos García-Ojeda ◽  
Inmaculada Martín-Burriel ◽  
Cendra Agulhon ◽  
Francisco Miana-Mena ◽  
...  
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Neurotrophic Factor ◽  
Tetanus Toxin ◽  
Brain Derived Neurotrophic Factor ◽  
Trophic Factors ◽  
Low Concentrations ◽  
Neuro2a Cells ◽  
Genetic Fusion ◽  
The Brain ◽  
Lateral Sclerosis

AbstractNeurotrophic factors have been widely suggested as a treatment for multiple diseases including motorneuron pathologies, like Amyotrophic Lateral Sclerosis. However, clinical trials in which growth factors have been systematically administered to Amyotrophic Lateral Sclerosis patients have not been effective, owing in part to the short half-life of these factors and their low concentrations at target sites. A possible strategy is the use of the atoxic C fragment of the tetanus toxin as a neurotrophic factor carrier to the motorneurons. The activity of trophic factors should be tested because their genetic fusion to proteins could alter their folding and conformation, thus undermining their neuroprotective properties. For this purpose, in this paper we explored the Brain Derived Neurotrophic Factor (BDNF) activity maintenance after genetic fusion with the C fragment of the tetanus toxin. We demonstrated that BDNF fused with the C fragment of the tetanus toxin induces the neuronal survival Akt kinase pathway in mouse cortical culture neurons and maintains its antiapoptotic neuronal activity in Neuro2A cells.

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