• Journal of Microbiology and Biotechnology
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• v.15 no.4
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• pp.838-843
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• 2005

Brain-derived neurotrophic factor (BDNF) is a small secretory protein and a member of the nerve growth factor (NGF) gene family. We cloned the flounder BDNF gene from a flounder brain cDNA library. The nucleotide sequence of the cloned gene showed an open reading frame (ORF) consisting of 810 bp, corresponding to 269 amino acid residues. The tissue distribution of flounder BDNF was determined by reverse transcription-polymerase chain reaction (RT-PCR) in brain, embryo, and muscle tissues. To express fBDNF using a eukaryotic expression system, we constructed the vector mpCTV-BDNF containing the fBDNF gene and transformed this vector into Chlorella ellipsoidea. Stable integration of introduced DNA was confirmed by PCR analysis of genomic DNA, and mRNA expression in C. ellipsoidae was confirmed by RT-PCR analysis.

• 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.

• Korean Journal of Biological Psychiatry
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• v.13 no.3
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• pp.162-169
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• 2006

Objective : Since some studies have shown that the brain-derived neurotrophic factor(BDNF) has an important role in the pathophysiology of depression, this study investigated the relationship between BDNF genetic polymorphism and the long-term outcome of the antidepressant treatment. Method : One hundred and eight patients with major depressive disorder were evaluated for the long-term outcome(up to 3 years) of antidepressant treatment. The severity and improvement of depression were assessed with the Clinical Global Impression(CGI) Scale. The genotypes of BDNF 196A/G polymorphism in the patients were determined using Restriction Fragment Length Polymorphism(RFLP). Result : The genotypes of 128 patients were investigated and 95 patients of those have been evaluated for 3 years. No significant differences were noted comparing three-genotype groups for CGI scales at baseline, 4 weeks, 8 weeks, 1 year, 2 years and 3 years. Conclusion : This result shows that BDNF polymorphism investigated in this study was not associated with the long-term outcome of the antidepressant treatment. However, further studies with another BDNF polymorphism should be needed.

• Physical Therapy Rehabilitation Science
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• v.11 no.3
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• pp.304-310
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• 2022

Objective: Mild cognitive impairment (MCI) is a condition in which cognitive and executive functions are reduced, and older adults with MCI are ten times more likely to develop dementia than healthy older adults. Expression of brain-derived neurotrophic factor (BDNF) through aerobic exercise is associated with increased cognitive and executive functions. in this review, randomized controlled trials (RCTs) on the effects of aerobic exercise on BDNF in individuals with mild cognitive impairment are summarized and qualitatively and quantitatively analyzed to suggest the necessity of aerobic exercise. Design: a systematic review and meta-analysis. Methods: RCTs were searched for changes in BDNF through aerobic exercise using four international databases. Quality assessment and quantitative analysis were performed using RevMan 5.4. Quantitative analysis was quantified with a standardized mean difference (SMD) and presented as a random effect model. Results: Three RCTs evaluated BDNF in 123 patients with MCI. There was a significant improvement in the experimental group that performed aerobic exercise compared to the control group. The results analyzed using the random effects model were SMD = 0.48. Conclusions: In this review, we reported the effects and mechanisms of aerobic exercise in individuals with MCI. As a result of synthesizing RCTs that performed aerobic exercise, a significant increase in BDNF was confirmed.

• Korean Journal of Biological Psychiatry
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• v.30 no.1
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• pp.1-6
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• 2023

Many psychiatric disorders are associated with brain functional dysfunctions and neuronal degeneration. According to the research so far, enhanced brain plasticity reduces neurodegeneration and recovers neuronal damage. Brain-derived neurotrophic factor (BDNF) is one of the most extensively studied neurotrophins in the mammalian brain that plays major roles in neuronal survival, development, growth, and maintenance of neurons in brain circuits related to emotion and cognitive function. Also, BDNF plays an important role in brain plasticity, influencing dendritic spines in the hippocampus neurogenesis. Changes in neurogenesis and dendritic density can improve psychiatric symptoms and cognitive functions. BDNF has potent effects on brain plasticity through biochemical mechanisms, cellular signal pathways, and epigenetic changes. There are pharmacological and non-pharmacological interventions to increase the expression of BDNF and enhance brain plasticity. Non-pharmacological interventions such as physical exercise, nutritional change, environmental enrichment, and neuromodulation have biological mechanisms that increase the expression of BDNF and brain plasticity. Non-pharmacological interventions are cost-effective and safe ways to improve psychiatric symptoms.

• Korean Journal of Biological Psychiatry
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• v.12 no.2
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• pp.216-220
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• 2005

Background:Brain-derived neurotrophic factor(BDNF) genes are thought to be important factors in some personality traits. The goal of this study was to determine the role of these genes in personality traits. Method:The participants included 170 healthy adults with no history of psychiatric disorders and other physical illnesses for the last 6 months. All participants were tested by the Temperament and Character Inventory (TCI). BDNF Val64Met gene polymorphisms were analyzed with PCR(Polymerase Chain Reaction). Differences on TCI dimensions and sub-scales among groups were examined with ANOVA. Result:There was a significant correlation between BDNF Val64Met and Persistence(PS)(p=0.036) in female subjects, but none with the other TCI dimensions. A post-hoc comparison revealed significant a difference between Val/Val and Met/Met (p=0.031). Conclusion:Our study suggests that the BDNF Val64Met gene polymorphism is associated with persistence in Korean female subjects, but the small number of subjects limits generalization of our results. Further studies with a larger number of homogenous subjects are needed to confirm whether the BDNF gene is related to personality traits.

• Journal of Korean Biological Nursing Science
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• v.4 no.1
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• pp.101-112
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• 2002

Peripheral nerve injury results in plastic changes in the dorsal ganglia (DRG) and spinal cord, and is often complicated with neuropathic pain. The mechanisms underlying these changes are not known, but these changes seem to be most likely related to the neurotrophic factors. This study investigated the effects of mechanical peripheral nerve injury on expression of brain-derived neurotrophic factor(BDNF) in the DRG and spinal cord in rats. 1) Bennett model and Chung model groups showed significantly increased percentage of small, medium and large BDNF-immunoreactive neurons in the ipsilateral $L_4$ DRG compared with those in the contralateral side at 1 and 2 weeks of the injury. 2) In the ipsilateral $L_5$ DRG of the Chung model, percentage of medium and large BDNF-immunoreactive neurons increased significantly at 1 week, whereas that of large BDNF-immunoreactive neurons decreased at 2 week when compared with those in the contralateral side. The intensity of immunoreactivity of each neuron was lower in the ipsilateral than in the contralateral DRG. 3) In the spinal cord, the Bennett and Chung model groups showed a markedly increased BDNF-immunoreactivity in axonal fibers of both superficial and deeper laminae. The present study demonstrates that peripheral nerve injury in neuropathic models altered the BDNF expression in the DRG and spinal cord. This may suggest important roles of BDNF in sensory abnormalities after nerve injury and in protecting the large-sized neurons in the damaged DRG.

• Korean Journal of Biological Psychiatry
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• v.11 no.2
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• pp.104-109
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• 2004

Objectives:Abnormalities in neurotrophic factors that regulate neuronal development and synaptic plasticity are often implicated as some causes of schizophrenia. In previous studies, researchers reported that brain and serum BDNF levels underwent similar changes during maturation and aging processes in rats. They also found a positive correlation between serum and cortical BDNF levels. In this study, we investigated whether the serum levels of BDNF in Korean schizophrenic patients would be different from those of healthy controls. Methods:Using an ELISA kit, serum BDNF levels were assessed in schizophrenic group(N=49) and control group(N=50). Results:Serum BDNF levels in the schizophrenic group($36.29{\pm}19.78$ng/ml) were significantly higher than those in control group($22.4{\pm}14.4$ng/ml). The BDNF levels did not correlate with duration of treatment, age or daily dose of antipsychotics in patients with schizophrenia. Conclusions:This result suggests that schizophrenia is characterized by high serum BDNF levels and supports the hypothesis of neurotrophic factor involvement in psychotic disorder. Serum BDNF level is likely to be one of the possible biological markers for schizophrenia.

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.6
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• pp.679-688
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• 2018

Autism spectrum disorders (ASDs) are neurodevelopmental disorders that share behavioral features, the results of numerous studies have suggested that the underlying causes of ASDs are multifactorial. Behavioral and/or neurobiological analyses of ASDs have been performed extensively using a valid model of prenatal exposure to valproic acid (VPA). Abnormal synapse formation resulting from altered neurite outgrowth in neural progenitor cells (NPCs) during embryonic brain development has been observed in both the VPA model and ASD subjects. Although several mechanisms have been suggested, the actual mechanism underlying enhanced neurite outgrowth remains unclear. In this study, we found that VPA enhanced the expression of brain-derived neurotrophic factor (BDNF), particularly mature BDNF (mBDNF), through dual mechanisms. VPA increased the mRNA and protein expression of BDNF by suppressing the nuclear expression of methyl-CpG-binding protein 2 (MeCP2), which is a transcriptional repressor of BDNF. In addition, VPA promoted the expression and activity of the tissue plasminogen activator (tPA), which induces BDNF maturation through proteolytic cleavage. Trichostatin A and sodium butyrate also enhanced tPA activity, but tPA activity was not induced by valpromide, which is a VPA analog that does not induce histone acetylation, indicating that histone acetylation activity was required for tPA regulation. VPA-mediated regulation of BDNF, MeCP2, and tPA was not observed in astrocytes or neurons. Therefore, these results suggested that VPA-induced mBDNF upregulation was associated with the dysregulation of MeCP2 and tPA in developing cortical NPCs.

• 한국생물공학회:학술대회논문집
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• 2003.04a
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• pp.743-746
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• 2003

The major pathological lesion in Parkinson's disease(PD) is selective degeneration and loss of pigmented dopaminergic neurons in substantia nigra (SN). Although the initial cause and subsequent molecular signaling mechanisms leading to the dopaminergic cell death underlying the PD process is elusive, the potent neurotrophic factors (NTFs), brain derived neurotrophic factor (BDNF) and glial cell line derived neurotrophic factor (GDNF), are known to exert dopaminergic neuroprotection both in vivo and in vitro models of PD employing the neurotoxin, MPTP. BDNF and its receptor, trkB are expressed in SN dopaminergic neurons and their innervation target. Thus, neurotrophins may have autocrine, paracrine and retrograde transport effects on the SN dopaminergic neurons. This study determined the BDNF secretion from SN dopaminergic neurons by ELISA. Regulation of BDNF synthesis/release and changes in signaling pathways are monitored in the presence of free radical donor, NO donor and mitochondrial inhibitors. Also, this study shows that BDNF is able to promote survival and phenotypic differentiation of SN dopaminergic neurons in culture and protect them against MPTP-induced neurotoxicity via MAP kinase pathway.