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      Decreased Plasma BDNF Levels of Patients with Somatization Disorder

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          Abstract

          Objective

          Brain-derived neurotrophic factor (BDNF), one of the most abundant and important neurotrophins, is known to be involved in the development, survival, maintenance, and plasticity of neurons in the nervous system. Some studies have suggested that BDNF may play a role in the pathophysiology of several psychiatric illnesses such as depression and schizophrenia. Similarly, it is likely that the alteration of BDNF may be associated with the neuro-modulation that contributes to the development of somatization disorder.

          Methods

          The purpose of this study was to determine whether there is an abnormality of plasma BDNF levels in patients with somatization disorder, and to analyze the nature of the alteration after pharmacotherapy using an enzyme-linked immunosorbent assay (ELISA).

          Results

          The plasma BDNF levels of the patients with a somatization disorder were significantly lower compared with those of the control volunteers (83.61±89.97 pg/mL vs. 771.36±562.14 pg/mL); moreover, the plasma BDNF levels of those patients who received an antidepressant were significantly increased after the treatment (118.13±91.45 pg/mL vs. 72.92±88.21 pg/mL).

          Conclusion

          These results suggest that BDNF may play a role in the pathophysiology of somatization disorder.

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          Most cited references52

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          Diagnostic and statistical manual of mental disorders.

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            Chronic antidepressant treatment increases neurogenesis in adult rat hippocampus.

            Recent studies suggest that stress-induced atrophy and loss of hippocampal neurons may contribute to the pathophysiology of depression. The aim of this study was to investigate the effect of antidepressants on hippocampal neurogenesis in the adult rat, using the thymidine analog bromodeoxyuridine (BrdU) as a marker for dividing cells. Our studies demonstrate that chronic antidepressant treatment significantly increases the number of BrdU-labeled cells in the dentate gyrus and hilus of the hippocampus. Administration of several different classes of antidepressant, but not non-antidepressant, agents was found to increase BrdU-labeled cell number, indicating that this is a common and selective action of antidepressants. In addition, upregulation of the number of BrdU-labeled cells is observed after chronic, but not acute, treatment, consistent with the time course for the therapeutic action of antidepressants. Additional studies demonstrated that antidepressant treatment increases the proliferation of hippocampal cells and that these new cells mature and become neurons, as determined by triple labeling for BrdU and neuronal- or glial-specific markers. These findings raise the possibility that increased cell proliferation and increased neuronal number may be a mechanism by which antidepressant treatment overcomes the stress-induced atrophy and loss of hippocampal neurons and may contribute to the therapeutic actions of antidepressant treatment.
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              Decreased serum brain-derived neurotrophic factor levels in major depressed patients.

              Recent findings with animal models have suggested a possible role for brain-derived neurotrophic factor (BDNF) in depression. We have therefore hypothesized that depression could be characterized by low levels of serum BDNF. Major depressed patients (15F + 15M) diagnosed according to DSM-IV criteria and healthy controls (15F + 15M) participated in the study. Serum BDNF was assayed with the ELISA method and the severity of depression was evaluated with Montgomery-Asberg-Depression Rating Scale (MADRS). BDNF levels were significantly lower in patients than in controls: 22.6 +/- 3 and 26.5 +/- 7 ng/ml (t-test = 2.7; d.f. = 58; P < 0.01). They were negatively correlated to the MADRS scores (r = -0.55; P < 0.02). Female patients were more depressed and released less BDNF than men. Analysis of covariance (MADRS and gender as independent variable vs. BDNF as dependent variable) indicated that depression severity mainly accounted for the negative correlation. These results suggest that major depression is characterized by low serum BDNF levels and support the hypothesis of neurotrophic factor involvement in affective disorders.
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                Author and article information

                Journal
                Psychiatry Investig
                Psychiatry Investig
                PI
                Psychiatry Investigation
                Korean Neuropsychiatric Association
                1738-3684
                1976-3026
                September 2016
                30 September 2016
                : 13
                : 5
                : 526-530
                Affiliations
                [1 ]Department of Psychiatry, Maeumsarang Hospital, Wanju, Republic of Korea.
                [2 ]Department of Psychiatry, Chonbuk National University Medical School, Jeonju, Republic of Korea.
                [3 ]Research Institute of Clinical Medicine of Chonbuk National University-Biomedical Research Institute of Chonbuk National University Hospital, Jeonju, Republic of Korea.
                [4 ]Department of Psychiatry, Korea University Ansan Hospital, Korea University College of Medicine, Ansan, Republic of Korea.
                Author notes
                Correspondence: Jong-Chul Yang, MD, PhD Department of Psychiatry, Chonbuk National University Medical School, 20 Geonji-ro, Deokjin-gu, Jeonju 54907, Republic of Korea Tel: +82-63-250-2580, Fax: +82-63-275-3157, yangjc@ 123456jbnu.ac.kr
                Correspondence: Yong-Ku Kim, MD, PhD. Department of Psychiatry, Korea University Ansan Hospital, Korea University College of Medicine, 122 Jeokgeum-ro, Danwon-gu, Ansan 15355, Republic of Korea. Tel: +82-31-412-5140, Fax: +82-31-412-5144, yongku@ 123456korea.ac.kr
                Article
                10.4306/pi.2016.13.5.526
                5067347
                27757131
                3bc8b44a-ecd3-4709-bd23-93be7d06de2c
                Copyright © 2016 Korean Neuropsychiatric Association

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 20 August 2015
                : 12 December 2015
                : 08 January 2016
                Funding
                Funded by: Chonbuk National University Hospital, CrossRef http://dx.doi.org/10.13039/501100002864;
                Categories
                Original Article

                Clinical Psychology & Psychiatry
                somatization disorder,bdnf,neurotrophin
                Clinical Psychology & Psychiatry
                somatization disorder, bdnf, neurotrophin

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