No abstract available.
Brain-Derived Neurotrophic Factor

No abstract available.
Abdominal Pain ; Brain-Derived Neurotrophic Factor ; Irritable Bowel Syndrome

OBJECTIVE: The aim of this study was to compare the serum brain-derived neurotrophic factor (BDNF) in acute depression with that in chronic depression. METHODS: Eighty subjects who met criteria for major depressive disorder (MDD) were recruited. Patients experiencing at least their fourth episode or an episode of at least 24 months in duration were defined as chronically depressed (n=21). Other patients were classified as acutely depressed (n=59). Antidepressant medications were administered for 6 weeks. Serum BDNF and Hamilton rating scale for depression (HAM-D) scores were measure before and after the administration of medication. RESULTS: We found significant differences in serum BDNF between the two groups. Serum BDNF was significantly higher among those with chronic depression than among those with acute depression both at baseline and after medication. CONCLUSION: This study suggested that serum BDNF might constitute a potential biological marker for chronic depression.
Biomarkers ; Brain-Derived Neurotrophic Factor ; Depression ; Depressive Disorder, Major ; Humans

Exercise is considered as one of the therapeutic options. in many major treatment guidelines for depression In terms of the underlying neurobiological mechanisms, it has been suggested that the antidepressive effects of exercise can be explained by the increased hippocampal volume associated with an increased level of brain-derived neurotrophic factor (BDNF). However, there have been no significant effects of exercise on cognitive functions in depression. Exercise has been used based on substantial evidence in the context of its therapeutic efficacy in depression. In personalized medicine, various potential mediators for the relationship between exercise and depressive symptoms should be controlled. Since it has been consistently reported that exercise has no significant therapeutic effects on cognitive domains in depression, it is necessary that the efficacy of exercise on cognitive domains should be evaluated with rigorous methodology. Furthermore, it has been suggested that exercise has potentially positive effects in the prevention of depression. Despite the controversies regarding supporting evidence, it is concluded that exercise may be regarded as a “safe and broad-spectrum antidepressant” and used in the context of “prevention and treatment of depression.”
Brain-Derived Neurotrophic Factor ; Cognition ; Depression ; Precision Medicine ; Therapeutic Uses

To investigate the relationship between anti-depressant effect and hippocampal nerve growth of Xiaoyao San,the inflammatory model of hippocampal neuron was induced by lipopolysaccharide( LPS). The effect of Xiaoyao San serum( final concentration of4%,8%) on the cell proliferation activity was detected by immunofluorescence,the levels of BDNF and β-NGF in the supernatant of hippocampal neurons were detected by ELISA,and the expressions of BDNF,NGF,Trk B,Trk A and CREB mRNA in cell lysate of hippocampal neuron were detected by PCR. Western blot was used to detect the expressions of Trk B,CREB,p-CREB and SYP protein in cell lysate of hippocampal neuron,and to reveal the neuroprotective effect and mechanism of Xiaoyao San. The results showed that8% Xiaoyao San serum could significantly increase in Brdu/Neu N ratio( P<0. 01). 4%,8% Xiaoyao San serum could significantly improve the levels of BDNF and β-NGF in supernatant( P<0. 05 or P<0. 01),up-regulate the expression of BDNF,NGF,Trk B,Trk A,CREB mRNA and Trk B,p-CREB,SYP protein in cell lysate( P< 0. 05 or P< 0. 01). 8% Xiaoyao San serum could significantly increase CREB protein in cell lysate( P<0. 05),and elevate in p-CREB/CREB ratio( P<0. 01). All the above results indicate that Xiaoyao San has a certain protective effect on LPS induced hippocampal neuron injury,which suggests that the protective effect of Xiaoyao San is related to the promotion of hippocampal nerve growth,which is one of its antidepressant mechanisms.
Brain-Derived Neurotrophic Factor ; Drugs, Chinese Herbal ; Hippocampus ; Lipopolysaccharides ; Neurons

Attention deficit hyperactivity disorder (ADHD) is a common childhood psychiatric disorder. Recently, it has been suggested that brain-derived neurotropic factor (BDNF) may play a role in the pathogenesis of ADHD. Our aim of this review is to understand the physiological functions of BDNF and its potential relationship with ADHD and therapeutic approaches of ADHD. Searches were conducted in Pubmed and Research Information Service System (RISS). In this review, we summarized important literatures for the physiological functions of BDNF in neurodevelopment, change of serum BDNF level in ADHD, association of BDNF polymorphism and ADHD and potential association of treatment of ADHD with serum BDNF level. Further studies are required to more clearly understand the source and the role of BDNF in ADHD and to develop BDNF based-ADHD treatement.
Attention Deficit Disorder with Hyperactivity* ; Brain-Derived Neurotrophic Factor ; Information Services

OBJECTIVE: Some clinical studies have found alterations in the levels of serum brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) after applying antidepressant treatment in patients with major depressive disorder (MDD). We evaluated the serum BDNF and GDNF levels before and after 12 weeks of antidepressant treatment in MDD outpatients. METHODS: Serum BDNF and GDNF levels were measured in 23 female MDD outpatients at baseline and after 12 weeks of treatment. The severity of depression was measured with the Hamilton Depression Rating Scale-17 (HAMD-17). Remission of MDD to the treatment was defined as a posttreatment HAMD-17 score of <7. RESULTS: Among MDD patients, 19 (82.6%) subjects were in mild to moderate depression. The whole MDD patients had significantly higher serum BDNF and GDNF levels at baseline than those after 12 weeks of antidepressant treatment. The baseline serum BDNF and GDNF levels did not significantly between the remission and nonremission groups. The significant alteration in both BDNF and GDNF levels after antidepressant treatment were observed in patients with remission. CONCLUSION: The present study suggests that the baseline serum BDNF and GDNF levels are higher than the posttreatment levels in some mild-to-moderate MDD outpatients and the significant alteration in BDNF and GDNF level after treatment were observed in patients with remission.
Brain-Derived Neurotrophic Factor* ; Depression ; Depressive Disorder, Major* ; Female* ; Glial Cell Line-Derived Neurotrophic Factor* ; Humans ; Outpatients*

OBJECTIVE: The aims of the present study were to explore the behavioural effects and to understand the possible mode of action of Bacopa monnieri extract (BME) on chronic unpredictable stress (CUS) induced depressive model and the biochemical alterations such as brain derived neurotrophic factor (BDNF), Akt, cyclic-AMP response element binding (CREB) protein level in the hippocampus of rats. METHODS: We examined the effects of chronic administration of BME on CUS exposed rats for 28 days. Behavioural changes were assessed by sucrose consumption and open field test to assess the effect of BME on CUS-induced depression. The mechanisms underlying antidepressant like action of BME was further evaluated by measuring levels of BDNF, Akt, and CREB in the hippocampus of rat brain and compared with the standard tricyclic antidepressant drug imipramine (20 mg/kg body weight). RESULTS: Exposure to CUS for 28 days produced depression-like behavior in rats, as indicated by significant decreases in sucrose consumption, locomotor activity including decreased BDNF, Akt and CREB levels in the hippocampus. Daily administration of BME at a dose of (80 mg/kg body weight) significantly reverses the behavioral alteration and restored the normal level of BDNF, total and phospho-Akt, total and phospho CREB in the hippocampus of CUS induced rats as compared to vehicle treated control rats. CONCLUSION: These findings suggest that BME ameliorates CUS induced behavioural depression in rats and that can be used as a potent therapeutic agent in treating depressive like behavior.
Animals ; Bacopa* ; Brain ; Brain-Derived Neurotrophic Factor* ; Depression ; Hippocampus* ; Imipramine ; Motor Activity ; Rats* ; Response Elements ; Sucrose

Brain-derived neurotrophic factor (BDNF) is linked to numerous brain functions. In addition, BDNF alterations contribute to neurological, mental, and addictive disorders. Cocaine dependence has received much attention recently due to its prevalence and psychological effects. Symptoms of psychosis are one of the most serious adverse events precipitated by cocaine use. It is particularly important to identify patients at risk of developing cocaine-induced psychosis (CIP). We described two cases of patients with cocaine dependence who presented with CIP and had changes in their BDNF levels during the psychotic episode. BDNF levels were initially low in both patients, and then decreased by more than 50% in association with CIP. The relationship between BDNF and psychosis is described in the literature. These cases revealed that BDNF levels decreased during a CIP episode and, thus, it is necessary to investigate BDNF and its relationship with CIP further.
Biomarkers ; Brain ; Brain-Derived Neurotrophic Factor ; Cocaine* ; Cocaine-Related Disorders* ; Humans ; Prevalence ; Psychotic Disorders*

Brain-derived neurotrophic factor (BDNF) is an important member of the neurotrophic factors, which are critical regulators of the formation and plasticity of neuronal networks. BDNF is abundant in the brain and periphery and it is found in both human serum and plasma. Stressed animals and depressed patients show reduced BDNF expression in the hippocampus and this reduction can be prevented by antidepressant drug treatment. Recent several clinical studies have indicated the decreases of serum or plasma BDNF levels in untreated patients with major depression. These decreases of BDNF can recover after antidepressant treatment. Increasing BDNF after antidepressant treatment could result from improving depressive symptoms, not just from antidepressant treatment. BDNF can play a critical role in the action mechanism of antidepressant treatment. Taken together, major depression may be considered a dysfunction of critical neuronal networks, and the gradual network recovery may induce antidepressant effect. Serum or plasma BDNF levels could indirectly show the above processes of major depression.
Animals ; Brain ; Brain-Derived Neurotrophic Factor ; Depression ; Hippocampus ; Humans ; Nerve Growth Factors ; Neurons ; Plasma ; Plastics