Association of the Brain-Derived Neurotrophic Factor and Serotonin Transporter Genes with Parameters of the Early Components of Event-Related Potentials on Passive Word Perception

2017 ◽  
Vol 47 (9) ◽  
pp. 1140-1146
Author(s):  
V. E. Golimbet ◽  
Zh. V. Garakh ◽  
G. I. Korovaitseva ◽  
T. V. Lezheiko ◽  
Yu. S. Zaitseva ◽  
...  
Keyword(s):  
Serotonin Transporter ◽  
Neurotrophic Factor ◽  
Event Related Potentials ◽  
Brain Derived Neurotrophic Factor ◽  
Word Perception ◽  
Related Potentials ◽  
The Brain

scholarly journals Cerebral 5-HT2A Receptor and Serotonin Transporter Binding in Humans Are Not Affected by the val66met BDNF Polymorphism Status or Blood BDNF Levels

2010 ◽  
Vol 30 (11) ◽  
pp. e1-e7 ◽  
Author(s):  
Anders Bue Klein ◽  
Viktorija Trajkovska ◽  
David Erritzoe ◽  
Steven Haugbol ◽  
Jacob Madsen ◽  
...  
Keyword(s):  
Serotonin Transporter ◽  
Receptor Binding ◽  
Neurotrophic Factor ◽  
Healthy Subjects ◽  
Brain Derived Neurotrophic Factor ◽  
Serotonergic System ◽  
Val66met Polymorphism ◽  
Serotonin System ◽  
Bdnf Val66met Polymorphism ◽  
The Brain

Recent studies have proposed an interrelation between the brain-derived neurotrophic factor (BDNF) val66met polymorphism and the serotonin system. In this study, we investigated whether the BDNF val66met polymorphism or blood BDNF levels are associated with cerebral 5-hydroxytryptamine 2A (5-HT2A) receptor or serotonin transporter (SERT) binding in healthy subjects. No statistically significant differences in 5-HT2A receptor or SERT binding were found between the val/val and met carriers, nor were blood BDNF values associated with SERT binding or 5-HT2A receptor binding. In conclusion, val66met BDNF polymorphism status is not associated with changes in the serotonergic system. Moreover, BDNF levels in blood do not correlate with either 5-HT2A or SERT binding.

Bringing the brain into personality assessment: Is there a place for event-related potentials?

2019 ◽  
Vol 31 (4) ◽  
pp. 488-501 ◽  
Author(s):  
Takakuni Suzuki ◽  
Kaylin E. Hill ◽  
Belel Ait Oumeziane ◽  
Dan Foti ◽  
Douglas B. Samuel
Keyword(s):  
Personality Assessment ◽  
Event Related Potentials ◽  
Related Potentials ◽  
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).

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