• Korean Journal of Biological Psychiatry
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• v.25 no.2
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• pp.21-30
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• 2018

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.

• Microbiology and Biotechnology Letters
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• v.25 no.1
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• pp.102-105
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• 1997

In cultivating human neuroblastoma cells maximum number of neurites per cell and length of the neurite were estimated as 5.5 and 2.2 (nm), respectively It was found that there was correlation between growth and differentiation of nerve cells. Maximum specific BDNF production rate was also calculated as 2.5$\times $10$^{-5}$(ng/cell/day) at 7$\times $ 10$^{5}$ (viable cells/ml) of maximum cell density, corresponding to 100 (ng/mL) of BDNF. The secretion of BDNF was occurred most in the later peroids of the cultivation, yielding 75 (ng/mL) of BDNF. The production of rate of BDNF was elongated in adding 1 ($\mu $g/mL) of BDNF as well as 40% increase of the length of the BDNF. It proves that BDNF can be used as one of biopharmaceuticals to treat age-related diseases such as Alzheimer's disease and Prakinson's disease. It can also provide the information of scaling-up mammalian cell cuture system to economically produce BDNF.

• Anxiety and mood
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• v.11 no.2
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• pp.129-135
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• 2015

Objective : Brain-derived neurotrophic factor (BDNF) is implicated in the pathophysiology of several neuropsychiatric disorders. However, there are few studies on BDNF of panic disorder. In this study, we investigated plasma BDNF levels in patients with panic disorder, and evaluated whether there are associations between clinical characteristics of panic disorder and plasma BDNF levels. Methods : We included 110 patients with panic disorder and 110 health controls in the current study. Plasma BDNF levels were measured by the enzyme-linked immunosorbent assay (ELISA). Plasma BDNF level differences were evaluated according to the clinical characteristics, such as duration of illness, recent stressful life event, agoraphobia, and insomnia. Results : The mean plasma BDNF levels of patients with panic disorder were significantly lower, as compared with those of controls (192.50 pg/mL vs. 693.75 pg/mL, t=8.838, p<0.001). The mean plasma BDNF levels of patients who had recent stressful life events were significantly higher, as compared with those who did not ($269.79{\pm}358.96pg/mL$ vs. $136.94{\pm}187.06pg/mL$, t=-2.525, p=0.013). Conclusion : These results suggested that BDNF plays a potential role in the pathophysiology of panic disorder.

• Korean Journal of Biological Psychiatry
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• v.16 no.3
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• pp.205-211
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• 2009

Objectives : Serum and plasma BDNF levels have been shown to be decreased in patients with mood disorder such as major depressive disorder and bipolar disorder. We investigated whether platelet BDNF levels would be lower in patients with acute bipolar manic episode compared with those of normal controls. Methods : BDNF levels were examined in platelet-rich plasma(PRP) and platelet-poor plasma(PPP) in 20 healthy controls and 20 hospitalized patients who were diagnosed as bipolar I disorder, most recent episode manic using a Structured Clinical Interview for DSM-IV. And severity of manic symptoms was measured using Young Mania Rating Scale(YMRS). Platelet BDNF level was calculated by subtracting PPP BDNF from PRP BDNF level, and dividing the result by the total platelet count, and it was expressed as pg/$10^6$ platelet. Results : Platelet BDNF levels were significantly lower in patients with acute bipolar manic episode(4.55${\pm}$3.36pg/$10^6$ platelet) than in normal controls(6.84${\pm}$2.32pg/$10^6$ platelet)(p=0.008). However we failed to reveal the significant negative correlation between platelet BDNF levels and YMRS scores in patients with acute bipolar episode. Conclusion : Our finding suggests that there is a decrease in the platelet BDNF of patients with acute bipolar manic episode.

• KSBB Journal
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• v.18 no.3
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• pp.207-210
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• 2003

The locus coeruleus (LC) contains about half of the total number of noradrenergic neurons in the brain and those noradrenergic neurons from the LC innervate entire brain regions. The LC is a major common target region in several neurodegenerative disorders such as Alzheimer's, Pakinson's and Huntington's diseases. The brain-derived neurotrophic factor (BDNF) regulate neuronal cell survival and differentiation of central nervous system neurons, including LC noradrenergic neurons. In this study, various small molecules and growth factors were tested as candidates to promote the production of BDNF in LC noradrenergic neuronal cells. The molecules tested include neuropeptides, cytokines, growth factors, neurotransmitters, and intracellular signaling agents. Four small molecules or growth factors, FGF8b, BMP-4, forskolin, and dibutyryl cGMP, were found to increase the release of BDNF in LC noradrenergic neurons. Especially, BMP-4 significantly enhanced BDNF production over 2.5-fold in LC noradrenergic neurons.

• Journal of Life Science
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• v.27 no.8
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• pp.879-887
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• 2017

It is well established that brain-derived neurotrophic factor (BDNF) is expressed not only in the brain but also in skeletal muscle, and is required for normal neuromuscular system function. Histone deacetylases (HDACs) and insulin-like growth factor-I (IGF-I) are potent regulators of skeletal muscle myogenesis and muscle gene expression, but the mechanisms of HDAC and IGF-I in skeletal muscle-derived BDNF expression have not been examined. In this study, we examined the effect of IGF-I and suberoylanilide hydroxamic acid (SAHA), a pan-HDAC inhibitor, on BDNF induction. Proliferating or differentiating C2C12 skeletal muscle cells were treated with increasing concentrations (0-50 ng/ml) of IGF-I in the absence or presence of $5{\mu}M$ SAHA for various time periods (3-24 hr). Treatment of C2C12 cells with IGF-I resulted in a dose- and time-dependent decrease in BDNF mRNA expression. However, inhibition of HDAC led to a significant increase in the expression of BDNF mRNA levels. In addition, immunocytochemistry revealed high BDNF protein levels in undifferentiated C2C12 skeletal muscle cells, whether untreated, IGF-I-treated, or exposed to SAHA. These results represent the first evidence that IGF-I can suppress the mRNA and protein expression of BDNF; conversely, SAHA attenuates the effects of IGF-I. Consequently, SAHA upregulates BDNF expression in C2C12 skeletal muscle cells.

• Polymer(Korea)
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• v.32 no.6
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• pp.529-536
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• 2008

We manufactured poly (L-lactide-co-glycolide) (PLGA) scaffolds impregnated demineralized bone particle (DBP) and hyaluronic acid (HA) by ice-particle leaching method and tested their ability of sustained release of brain derived neurotrophic factor (BDNF). BDNF (50 and 200 ng) mixed with PLGA, DBP/PLGA, HA/PLGA and DBP/HA/PLGA scaffold. The release profiles of BDNF from BDNF loaded scaffolds were assayed using ELISA. Morphological changes of scaffolds by BDNF release were also observed by SEM. BDNF stably and sustainedly released from DBP/HNPLGA than from PLGA and DBP/PLGA scaffolds. DBP/HA/PLGA scaffolds showed the great structural changes, which demonstrated BDNF release amount from DBP/HA/PLGA scaffolds were highest in all groups. We suggest that BDNF loaded DBP/HNPLGA scaffold would be very useful for nerve regeneration.

• Korean Journal of Biological Psychiatry
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• v.13 no.4
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• pp.267-272
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• 2006

Objectives : Schizophrenia is a clinically heterogenous disease with a strong genetic component. Many studies have suggested that brain-derived neurotrophic factor(BDNF) is involved in the pathophysiology of schizophrenia. This study was performed to determine whether there is an association between BDNF Val66Met polymorphism and schizophrenia. Methods : To identify any genetic predisposition to schizophrenia, we investigated the BDNF Val66Met polymorphism in 106 patients with schizophrenia and 147 normal controls with PCR-RFLP method. Statistical analyses were used to test the association between and BDNF Val66Met genotype and Schizophrenia. Results : No association was found between BDNF Val66Met polymorphism and schizophrenia. No significant differences were found comparing the BDNF genotype distributions according to the age of onset, the number of admission and familial loading in schizophrenia. Conclusion : This result indicates that BDNF Val66Met polymorphism is not associated with schizophrenia. However, further studies with a large number of subjects are needed to confirm whether the BDNF gene is related to schizophrenia.

• The Journal of the Korea Contents Association
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• v.19 no.2
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• pp.558-567
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• 2019

This study examined the effects of complex dance program(ballet, contemporary dance, yoga) on the body composition, BDNF, and serotonin of delivery women, by providing this program for 12 weeks to 14 women(within one year delivery: seven woman, 1-3 years after delivery: seven women). In the results of body composition, in the main effects in accordance with period, both groups showed significant decreases of body fat percentage. The fat-free mass was significantly increased in the group of women within one year after childbirth(t=3.821, p=.009). Regarding BDNF and serotonin, there were no interactive effects between groups and periods while the main effects did not show differences between groups and periods(p>.05). In the results of correlation analysis and regression analysis on BDNF, body composition, and serotonin, the BDNF and serotonin showed the positive correlation(p=.025). In the results of simple regression analysis, the explanatory power was 17.9%(r=.424, $r^2=.179$).

• PNF and Movement
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• v.4 no.1
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• pp.51-62
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• 2006

Purpose : The purposes of this study were to test the effect of proprioceptive and vestibular sensory input on expression of BDNF after traumatic brain injury in the rat. Subject : The control group was sacrificed at 24 hours after traumatic brain injury. The experimental group I was housed in standard cage for 7 days. The experimental group II was housed in standard cage after intervention to proprioceptive and vestibular sensory(balance training) for 7 days. Method : Traumatic brain injury was induced by weight drop model and after operation they were housed in individual standard cages for 24 hours. After 7th day, rats were sacrificed and cryostat coronal sections were processed individual1y in goat polyclonal anti-BDNF antibody. The morphologic characteristics and the BDNF expression were investigated in injured hemisphere section and contralateral brain section from immunohistochemistry using light microscope. Result : The results of this experiment were as follows: 1. In control group, cell bodies in lateral nucleus of cerebellum, superior vestibular nucleus, purkinje cell layer of cerebellum and pontine nucleus changed morphologically. 2. The expression of BDNF in contralateral hemisphere of group II were revealed. 3. On 7th day after operation, immunohistochemical response of BDNF in lateral nucleus, superior vestibular nucleus, purkinje cell layer and pontine nucleus appeared in group II. Conclusion : The present results revealed that intervention to proprioceptive and vestibular sensory input is enhance expression of BDNF and it is useful in neuronal reorganization improvement after traumatic brain injury.