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1.
Ghanshyam N. Pandey Yogesh Dwivedi Hooriyah S. Rizavi Xinguo Ren Hui Zhang Mani N. Pavuluri 《Progress in neuro-psychopharmacology & biological psychiatry》2010
Background
Brain-derived neurotrophic factor (BDNF) is a member of a neurotrophin family and is involved in many physiological functions, including cell proliferation, migration, and differentiation, and neuron survival in the human nervous system. Abnormalities of BDNF have been implicated in the pathophysiology of depression based on observations that antidepressant drugs cause increases in the levels of BDNF in rat brains and its abnormalities have appeared in the serum of depressed patients and in postmortem brains of suicide victims.Methods
We examined the gene expression of BDNF in the lymphocytes and protein expression in the platelets of adult and pediatric depressed patients during a drug-free period. We determined BDNF gene expression using a quantitative RT-PCR method and protein expression using the ELISA method.Results
We observed that the gene expression of BDNF was significantly decreased in the lymphocytes of adult and pediatric depressed patients compared with normal control subjects. Similarly, the protein expression of BDNF was significantly decreased in the platelets of adult and pediatric depressed patients compared with normal control subjects.Conclusions
To our knowledge, this is the first study that reports a decrease in BDNF gene expression in the peripheral cells of depressed patients. Because of the bidirectional movement of BDNF between the periphery and the CNS, the reduced gene expression in the lymphocytes and the protein expression in the platelets may be an index of similar abnormalities in the brain and could be a target for antidepressant drugs. 相似文献2.
Ayşe Devrim Başterzi Kemal Yazici Visal Buturak Burak Çimen Aylin Yazici Gülçin Eskandari Şenel Tot Acar Bahar Taşdelen 《Progress in neuro-psychopharmacology & biological psychiatry》2010
Background
Studies have yielded conflicting results concerning flow cytometric lymphocyte analyses in patients with depression. Data about the effect of antidepressants on lymphocyte subsets are also contradictory. The aim of this study was to determine effects of venlafaxine versus fluoxetine on lymphocyte subsets in depressive patients.Methods
Sixty-nine patients diagnosed with major depressive disorder (MDD) according to DSM-IV and 36 healthy controls are included in the study. Sixty-nine patients were randomized to take fluoxetine (FLX) (n = 33) or venlafaxine (VEN) (n = 36). Serum lymphocyte subsets included CD3, CD4, CD8, CD16/56, CD19, CD45, Anti-HLA-DR which were measured by flow cytometric analyses at baseline and 6 weeks after the start of treatment. The severity of depression was evaluated with Hamilton rating scale for depression.Results
At baseline, patients with MDD had significantly lower CD16/56 ratio and higher CD45 ratio compared to the controls. Although numerically higher in the VEN treated patients, treatment response rates between the FLX (53%) and the VEN (75%) groups were not different statistically. CD45 values decreased significantly in the VEN group at the end of the 6 week treatment period whereas no difference was observed in the FLX group. By the 6th week, treatment responders showed a significantly higher CD16/56 ratio than non-responders. Baseline severity of depression and anxiety was positively correlated with baseline CD45 ratio and negatively correlated with baseline CD16/56 ratio. We did not observe consistent changes in the absolute number of circulating B or T cells, nor in the helper/inducer (CD4) or suppressor/cytotoxic (CD8) subsets.Conclusions
CD16/56 was lower in patients with MDD and increased in treatment responders at 6th week. CD45 ratio was higher in patients with MDD than healthy subjects; it decreased with antidepressant treatment and was positively correlated with the severity of depression. Antidepressant treatment contributes to immune regulation in patients with major depressive disorder. 相似文献3.
Reiji Yoshimura Taro Kishi Hikaru Hori Asuka Katsuki Atsuko Sugita-Ikenouchi Wakako Umene-Nakano Kiyokazu Atake Nakao Iwata Jun Nakamura 《Psychiatry investigation》2014,11(1):84-88
Objective
It is important to predict a response to an antidepressant in early time after starting the antidepressant. We previously reported that serum brain-derived neurotrophic factor (BDNF) levels in responders to treatment with antidepressants were increased, whereas, those in nonresponders were not. Therefore, we hypothesized that the changes in serum levels of BDNF from baseline (T0) to 4 weeks (T4) after treatment with selective serotonin reuptake inhibitors (SSRIs) predict the response to the treatment at 8 weeks (T8) in depressed patients. To confirm the hypothesis, we measured serum BDNF at T0, T4, and T8 during the treatment with SSRIs (paroxetine, sertraline, and fluvoxamine).Methods
One hundred fifty patients (M/F; 51/99, age; 50.4±15.1 years) met major depressive disorder (MDD) using by DSM-IV-TR enrolled in the present study. We measured serum BDNF concentrations at T0, T4, and T8 in patients with MDD treated with SSRIs.Results
The changes in serum BDNF, age, sex, dose of SSRIs, and HAMD-17 score did not predict the response to SSRIs at T8.Conclusion
These results suggest that the changes in serum BDNF levels from T0 to T4 could not predict the subsequent responses to SSRIs at T8. 相似文献4.
William Berger Akhil Mehra Maryann Lenoci Thomas J. Metzler Christian Otte Gary Tarasovsky Synthia H. Mellon Owen M. Wolkowitz Charles R. Marmar Thomas C. Neylan 《Progress in neuro-psychopharmacology & biological psychiatry》2010
Introduction
Some studies have found that antidepressants increase serum brain-derived neurotrophic factor (BDNF) levels in patients with major depression and the expression of BDNF mRNA in limbic structures of rats.Objectives
This study addressed whether the SSRI escitalopram increases serum BDNF levels in subjects with PTSD and whether BDNF levels are associated with treatment response.Methods
Medically healthy male subjects (N = 16) with chronic PTSD completed a 12 week open-label trial of flexible dose (5–20 mg/day) escitalopram monotherapy. BDNF levels were obtained at baseline, and at weeks 4, 8 and 12.Results
PTSD symptoms significantly declined over the course of the 12 week escitalopram treatment. Despite a substantial improvement in PTSD symptoms, there was virtually no change in BDNF levels over time. Nevertheless, mean BDNF levels across the trial were strongly correlated with the slope of PTSD symptoms over the 12 weeks (r = 0.58, p = 0.018). Lower mean BDNF was associated with a greater decrease in PTSD symptoms over the course of the trial.Conclusions
PTSD subjects with low BDNF levels demonstrated the largest treatment response from an agent with putative neurotrophic effects. 相似文献5.
Wolkowitz OM Wolf J Shelly W Rosser R Burke HM Lerner GK Reus VI Nelson JC Epel ES Mellon SH 《Progress in neuro-psychopharmacology & biological psychiatry》2011,35(7):1623-1630
Objectives
The “neurotrophin hypothesis” of depression posits a role of brain-derived neurotrophic factor (BDNF) in depression, although it is unknown whether BDNF is more involved in the etiology of depression or in the mechanism of action of antidepressants. It is also unknown whether pre-treatment serum BDNF levels predict antidepressant response.Methods
Thirty un-medicated depressed subjects were treated with escitalopram (N = 16) or sertraline (N = 14) for 8 weeks. Twenty-five of the depressed subjects completed 8 weeks of antidepressant treatment and had analyzable data. Twenty-eight healthy controls were also studied. Serum for BDNF assay was obtained at baseline in all subjects and after 8 weeks of treatment in the depressed subjects. Depression ratings were obtained at baseline and after 8 weeks of treatment in the depressed subjects.Results
Pre-treatment BDNF levels were lower in the depressed subjects than the controls (p = 0.001) but were not significantly correlated with pre-treatment depression severity. Depression ratings improved with SSRI treatment (p < 0.001), and BDNF levels increased with treatment (p = 0.005). Changes in BDNF levels were not significantly correlated with changes in depression ratings. However, pre-treatment BDNF levels were directly correlated with antidepressant responses (p < 0.01), and “Responders” to treatment (≥ 50% improvement in depression ratings) had higher pre-treatment BDNF levels than did “Non-responders” (p < 0.05).Conclusions
These results confirm low serum BDNF levels in un-medicated depressed subjects and confirm antidepressant-induced increases in BDNF levels, but they suggest that antidepressants do not work simply by correcting BDNF insufficiency. Rather, these findings are consistent with a permissive or facilitatory role of BDNF in the mechanism of action of antidepressants. 相似文献6.
Simone Hauck Flávio Kapczinski Rafael Roesler Érico de Moura Silveira Jr. Pedro V. Magalhães Letícia Rosito Pinto Kruel Sidnei Samuel Schestatsky Lúcia Helena Freitas Ceitlin 《Progress in neuro-psychopharmacology & biological psychiatry》2010
Objective
Brain-derived neurotrophic factor (BDNF) has an important role in learning, motivation and regulation of mood. The aim of this study was to investigate levels of serum BDNF in patients with trauma psychopathology (acute and post-traumatic stress disorder) when compared to age and gender matched controls.Method
A consecutive sample of 34 patients was evaluated regarding socio-demographic and clinical variables by means of a standard protocol, Davidson Trauma Scale, Beck Depression Inventory, Clinical Global Impression and the Global Assessment of Functioning. BDNF serum levels were measured right after the intake interview.Results
Patients had higher BDNF levels than controls. Those levels, however, were higher right after the traumatic event, decreasing over time. When two groups of patients (recent and remote trauma) were investigated in separate, the recent trauma group (less than 1 year since the traumatic event) had higher BDNF than controls, but this effect was not detected in the remote trauma group. The recent and remote trauma groups had different BDNF levels. Those findings persisted, even controlling for symptom severity, use of psychotropic medication, and history of psychiatric disease.Conclusions
As far as we know this is the first report of elevated serum BDNF levels in patients with recent trauma. Based in animal models that implicate BDNF in memory formation and consolidation, higher BDNF in recent PTSD could be related to memory and learning disruption central in PTSD psychopathology. 相似文献7.
Yan-Li Luo Ming-Yuan Zhang Wen-Yuan Wu Chun-Bo Li Zheng Lu Qing-Wei Li 《Progress in neuro-psychopharmacology & biological psychiatry》2009
Objectives
To verify the efficacy and safety of fluoxetine in treating patients with persistent somatoform pain disorder (PSPD).Methods
In this 8-week, randomized double-blind placebo-controlled study, 80 patients with an ICD-10 diagnosis of PSPD were randomly assigned to receive 20 mg fluoxetine or a placebo. Several psychological scales including Medical Outcomes Study Pain Measures (MOSPM), Hamilton Depression Scale-17 items (HAMD17) and Treatment Emergent Symptom Scale (TESS) were used to assess analgesic efficacy and safety of fluoxetine, and the possible analgesic mechanism of fluoxetine was preliminarily analyzed. All data were analyzed by SPSS11.5 with t-test, one-way ANOVA and a mixed-effects model repeated measures analysis. Intent-to-treat (ITT) analysis was performed and the last observation carry forward (LOCF) was used for missing values.Results
There was a significant difference of MOSPM total score between the fluoxetine and placebo group after 2 weeks of treatment. The analgesic effect of fluoxetine was related with treatment time, and depressive patients showed a better analgesic effect than non-depressive patients. An adverse effect of fluoxetine was scarcely found.Conclusions
Fluoxetine has a better analgesic effect than a placebo in treating persistent somatoform pain disorder, and is considered a safe treatment; its analgesic effect may be related to an antidepressant effect. 相似文献8.
Satoshi Saito Kimihiko WatanabeEri Hashimoto Toshikazu Saito 《Progress in neuro-psychopharmacology & biological psychiatry》2009
Background
Several lines of evidence suggest that brain-derived neurotrophic factor (BDNF) plays an important role in weight regulation and eating behavior, and poorly balanced diets lead to a decrease in blood BDNF levels. However, studies regarding BDNF blood levels in eating disorders (ED) have yielded inconsistent results. We measured serum concentrations of BDNF and assessed behavior and cognition related to eating in ED patients and control subjects.Methods
Forty female drug-free patients [19 with anorexia nervosa (AN), 21 with bulimia nervosa (BN)], who did not meet the diagnostic criteria for depressive disorder, and 24 age-matched normal control subjects were enrolled in the current study. We evaluated eating-related psychopathology and depressive symptoms using the Eating Disorder Inventory-2 (EDI-2), Eating Attitude Test-26 (EAT-26) and the Hamilton Depression Rating Scale (HDRS), and measured serum BDNF levels by an enzyme-linked immunosorbent assay.Results
Compared to normal controls, serum levels of BDNF were significantly reduced in AN, but not in BN. There was a significant positive correlation between serum BDNF levels and BMI in both AN patients (r = .649, p = .003) and BN patients (r = .626, p = .002). However, no correlation between serum BDNF levels and BMI was detected in the controls. Furthermore, there was a significant negative correlation between serum BDNF levels and the oral control subscale scores of EAT in both AN patients (r = − .506, p = .027) and BN patients (r = − .511, p = .018); whereas, no correlation was detected in normal controls.Conclusion
Our study demonstrated that individuals showing more extreme food intake regulation were those with lower serum BDNF levels. This finding is contrary to that in mice where mice with reduced BDNF levels showed aberrant eating behavior. This result suggests that BDNF is no longer functioning appropriately in ED patients, which could be an important factor in the pathophysiological of ED. 相似文献9.
The effect of chronic antidepressant treatment on serum brain-derived neurotrophic factor levels in depressed patients: a preliminary study 总被引:11,自引:0,他引:11
Aydemir O Deveci A Taneli F 《Progress in neuro-psychopharmacology & biological psychiatry》2005,29(2):261-265
Recent studies suggested a role of brain-derived neurotrophic factor (BDNF) in depression. While BDNF levels are lower in depressed patients, antidepressant treatment increases serum BDNF levels of depressed patients. Our study aims to test the effect of chronic venlafaxine treatment on serum BDNF levels in patients with a major depressive disorder. Ten patients diagnosed as major depressive disorder according to DSM-IV are included in the study. Two of the patients had their first episode and were drug-naive, the other eight patients were drug-free for at least 4 weeks. The severity of depression was assessed with Hamilton Depression Rating Scale (HDRS). The control group consisted of ten age- and sex-matched subjects without any psychiatric disorder. Blood samples were collected at the baseline and after 12 weeks of antidepressant treatment (during remission). At the baseline the mean serum BDNF level was 17.9+/-9.1 ng/ml and the mean HDRS score was 23.2+/-4.6. Serum BDNF levels of the study group were significantly lower than in the control group (31.6+/-8.6 ng/ml). At the end of the study, the mean serum BDNF level was 34.6+/-7.1 ng/ml whereas the mean HDRS score was 8.2+/-3.9. From the baseline to the remission after 12 weeks of treatment, the increase in serum BDNF level and the decrease in HDRS score were statistically significant, respectively. When we compared the serum BDNF level of depressed patients at remission to that of the controls, there was no statistically significant difference. This study shows that venlafaxine treatment of depression improves serum BDNF level which may be considered as a nonspecific peripheral marker of depression. 相似文献
10.
Objective
We assessed major cognitive domains in major depressive disorder (MDD) compared to a healthy control group using neurocognitive tests. We hypothesized that lower serum brain-derived neurotrophic factor (BDNF) levels would be associated with poorer neurocognitive performance in patients with major depression and that these associations would be shown in healthy controls as well.Method
Executive functions, sustaining and focusing of attention, memory functions, and verbal fluency were assessed in this study using the Trail-Making Test (TMT), Stroop Color Word Interference Test-TBAG Form (SCWT), Wisconsin Card Sorting Test (WCST), Test of Variables of Attention (TOVA), Auditory Consonant Trigram test (ACTT), Digit Span subtest of the Wechsler Memory Scale (DST), Rey Auditory Verbal Learning Test (RAVLT), and Controlled Oral Word Association Test (COWAT).Results
The MDD group showed significantly poorer performance than the control group in cognitive functions; they also had lower levels of BDNF than the control group. However, there was no correlation between cognitive performances and BDNF levels except in the TMT, Part B.Conclusions
The current understanding of the importance of neurocognitive assessment and related biological markers in depression is improving. Further studies with larger sample sizes evaluating neurocognitive functions with molecular analyses of BDNF levels may reveal a novel marker for predicting and monitoring neurocognitive deficits in depression. 相似文献11.
Luis Pintor Xavier Torres Victor Navarro M Jesús Martinez de Osaba Silvia Matrai Cristobal Gastó 《Progress in neuro-psychopharmacology & biological psychiatry》2009
Purpose
To study the power of CRF stimulation test to predict relapse in a sample of melancholic depressive patients in depressed phase, followed-up over a two-year period from the moment they achieved complete remission of depressive symptoms.Methods
Fifty-one outpatients diagnosed with unipolar depressive disorder with melancholic features according to DSM-IV were assessed with the CRF test. The Structured Clinical Interview for DSM-IV (SCID-IV) was used for diagnosis. Monthly follow-up visits were held over a two-year period after remission; relapse was established using HDRS according to Frank's criteria [Frank E, Prien RF, Jarret RB, Keller MB, Kupfer DJ, Lavori PW, et al. Conceptualization and rationale for consensus definitions of terms in major depressive disorder: remission, recovery, relapse, and recurrence. Arch Gen Psychiatry 1991;48:851–5]. Forty-three patients completed the study. Non-controlled antidepressant treatment protocols were used. Predictive statistical analysis was performed through logistic regression.Findings
The final predictive model included three variables: net area under cortisol curve (NAUCC), previous suicide attempt, and stress during follow-up. Sensitivity was of 89%, and specificity was of 92%. NAUCC has shown a predictive power of 80%, with an optimal cut-off point of 251.24 μg/ml/min.Conclusions
Cortisol is the hormone of the HPA axis which shows the highest power to predict relapse. NAUCC is the most relevant variable. The complete predictive model is a complex combination of biological, clinical and psychoenvironmental variables (NAUCC, previous suicide attempts, and stress during follow-up). Further studies with better control of the psychoenvironmental variables are required to obtain more precise neuroendocrine findings. 相似文献12.
Background
Brain derived neurotrophic factor (BDNF) has been implicated in the pathophysiology of depression and the antidepressant response. Electroconvulsive therapy (ECT) is reported to increase BDNF levels in blood, though only a small number of studies have been conducted to date.Objective
Our objectives were to: 1) compare plasma BDNF levels in medicated patients with depression and controls; 2) assess the effect of ECT on plasma BDNF levels in medicated patients with depression; 3) explore the relationship between plasma BDNF levels and the Val66Met (rs6265) BDNF polymorphism; and 4) examine the relationship between plasma BDNF levels and clinical symptoms and outcomes with ECT.Methods
Plasma BDNF levels were analyzed in samples from 61 medicated patients with a major depressive episode and 50 healthy controls, and in patient samples following a course of ECT. Fifty-two samples from the depressed patient group were genotyped for the Val66Met BDNF polymorphism.Results
There was no difference in plasma BDNF levels between the control and depressed groups, and there was no difference in plasma BDNF levels in patients following treatment with ECT. In line with previous reports, we show that, in medicated patients with depression, Met-carriers had higher plasma BDNF levels than Val-carriers, though genotype was not related to clinical response. We found no association between plasma BDNF levels and depression severity or the clinical response to ECT.Conclusions
Our results suggest that plasma BDNF does not represent a suitable candidate biomarker for determining the therapeutic response to ECT. 相似文献13.
Cemil Celik Murat Erdem Tuncer Caycı Barbaros Ozdemir E. Ozgur Akgul Yasemin Gulcan Kurt Halil Yaman Mehmet Isıntas Fuat Ozgen Aytekin Ozsahin 《Progress in neuro-psychopharmacology & biological psychiatry》2010
Background
There is an interaction between the immune system and the central nervous system by means of hormones, peptides, and neurotransmitters. The aims of the present study were to determine whether the serum neopterin levels in patients with major depression (MD) differ from a healthy control group and to investigate the relationship between previous MD episodes and serum neopterin levels.Methods
Thirty patients who were admitted to the GATA Psychiatry Outpatient Clinics and were diagnosed with MD according to DSM-IV, and who agreed to participate in the study, were included in the study. Twenty-six healthy volunteers matched for age, gender, and level of education who agreed to participate in the study were served as controls. Peripheral venous blood samples were obtained from the patients and the control group for complete blood count, routine biochemistry, and the detection of serum neopterin levels. The analyses were performed in the laboratory of the GATA Department of Biochemistry.Results
There was no significant difference between the MD group and the healthy controls with respect to age, level of education, smoking, and gender. Serum neopterin levels of the MD group who had experienced two or more episodes were higher than the first-episode group and the control group. Age of onset and the number of previous episodes had an independent impact on serum neopterin levels in MD patients, while smoking did not show any effect.Conclusion
In the present study, the neopterin levels of patients who had experienced two or more episodes were higher than the first-episode depressive group and healthy control group. It was also found that the number of previous depressive episodes and the ages of the MD cases had an independent effect on serum neopterin levels. 相似文献14.
Huirong Zheng Li Zhang Lingjiang Li Peng Liu Junling Gao Xiaoyun Liu Juan Zou Yan Zhang Jun Liu Zhijun Zhang Zexuan Li Weiwei Men 《Progress in neuro-psychopharmacology & biological psychiatry》2010
Background
Neuroimaging studies suggest that the prefrontal cortex (PFC) is involved in the pathophysiology of major depression. Repetitive transcranial magnetic stimulation (rTMS) as an antidepressant intervention has increasingly been investigated in the last two decades. In this study metabolic changes within PFC of severely depressed patients before and after rTMS were evaluated by proton magnetic resonance spectroscopy (1H-MRS).Method
Thirty-four young depressed patients with treatment-resistant unipolar depression were enrolled in a double-blind, randomized study〔active ((n = 19) vs. sham(n = 15)), and the PFC was investigated before and after high-frequency (15 Hz) rTMS using 3-tesla proton magnetic resonance spectroscopy. Response was defined as a 50% reduction of the Hamilton depression rating scale. The results were compared with 28 age- and gender-matched healthy controls.Results
In depressive patients a significant reduction in myo-inositol (m-Ino) was observed pre-rTMS (p < 0.001). After successful treatment, m-Ino increased significantly in left PFC and the levels no longer differed from those of age-matched controls. In addition to a positive correlation between clinical improvement and an increment in m-Ino ratio, a correlation between clinical improvement and early age onset was observed.Conclusions
Our results support the notion that major depressive disorder is accompanied by state-dependent metabolic alterations, especially in myo-inositol metabolism, which can be partly reversed by successful rTMS. 相似文献15.
Jianting Huang Xuanwei Liu Xun Luo Chunzhi Tang Mingzhu Xu Lisa Wood Yulong Wang Qing Mei Wang 《Journal of stroke and cerebrovascular diseases》2018,27(11):3320-3327
Background
To investigate whether fluoxetine improves poststroke dysphagia and to detect the potential relationship between serum brain-derived neurotrophic factor (BDNF) levels and fluoxetine effects.Methods
In this retrospective study, 159 stroke patients who met our study criteria were included. In total, 110 patients were placed in the control group, and 49 patients were placed in the fluoxetine group. Demographic and clinical characteristics of the patients were collected for the baseline assessment. Functional independence measure scores and American speech-language-hearing association/functional communication measures scores for swallowing were collected to evaluate the patients’ swallowing function. Patients’ serums were collected at weeks 1 and 3 after admission, and serum BDNF levels were measured by enzyme-linked immunosorbent assay. T test, chi-squared test, and general linear model analysis were performed to determine the differences between the two groups.Results
A significantly higher improvement of swallowing function was observed in the fluoxetine group compared with that of the control group (P?=?.023). In addition, a general linear model analysis showed that the treatment of fluoxetine has a statistically significant effect on swallowing improvement after adjustment of swallowing score on admission, stroke types, and interval between the onset of stroke and admission (P?=?.022, R2?=?.46, adjusted R2?=?.446). There is no significant difference in the change of serum BDNF levels in the two groups (P?=?.269).Conclusions
This study suggests that treatment with fluoxetine in stroke patients with dysphagia may improve swallowing function. A placebo-controlled, randomized clinical trial is warranted to confirm this finding. 相似文献16.
Marlijn Vermeiden Paul G. Mulder Walter W. van den Broek Jan A. Bruijn Tom K. Birkenhäger 《Journal of psychiatric research》2013
Objective
To compare the efficacy of plasma level-targeted dose imipramine and high-dose venlafaxine in depressed inpatients in a randomized double-blind study.Methods
The study included 85 patients with a diagnosis of major depressive episode according to the DSM IV criteria and a 17-item Hamilton Rating Scale for Depression (HAM-D) score ≥ 17.Patients were randomized to imipramine or venlafaxine. The dose of imipramine was adjusted for each patient to a predefined blood level of 200–300 ng/ml. The dose of venlafaxine was increased gradually to 300–375 mg/day. Efficacy was evaluated after 7 weeks of treatment.Results
The mean age of the study group was 54.5 (range 29–82) years. There was no significant difference according to the primary outcome criterion of a ≥50% reduction on the HAM-D score: 17 of 43 (39.5%) patients on imipramine were responders compared to 21 of 42 (50%) patients on venlafaxine. When considering remission as outcome criterion (HAM-D score ≤ 7), 10 of 43 (23.3%) patients on imipramine were remitters compared to 15 of 42 (35.7%) patients on venlafaxine; again, no significant difference. When analysing a subpopulation of patients without psychotic features, with remission as outcome criterion, a significant difference was found: 5 of 34 (14.7%) patients on imipramine were remitters compared to 12 of 31 (38.7%) patients on venlafaxine.Conclusions
The present study used optimal doses in depressed inpatients and showed that venlafaxine is at least equal in efficacy to imipramine. The results in the subgroup without psychotic features indicate a possible superiority of venlafaxine. 相似文献17.
Byong-Su Jang Hyeran Kim Shinn-Won Lim Ki-Won Jang Doh-Kwan Kim 《Psychiatry investigation》2008,5(3):193-198
Objective
S100B is a neurotrophic factor that is involved in neuroplasticity. Neuroplasticity is disrupted in depression; however, treatment with antidepressants can restore neuroplasticity. S100B has previously been used as a biological marker for neuropathology and neuroplasticity; therefore, in this study, we compared serum S100B levels in depressive patients to those of normal controls. In addition, we compared the serum S100B levels of antidepressant responders to those of nonresponders.Methods
Thirty five normal controls and 59 depressive patients were enrolled in this study. Depressive patients entered a 6 week clinical trial that included treatment with antidepressants. The serum S100B levels and clinical assessments, which included Hamilton depression rating scores, were measured at baseline and after 6 weeks of treatment with antidepressants. The difference in the serum S100B levels between depressive patients and normal controls and between antidepressant responders and nonresponders was then compared.Results
There were no significant differences in the serum S100B levels of normal controls and depressive patients. In addition, 30 of the depressive patients responded to antidepressant treatment while 29 did not. Finally, the responders had significantly higher baseline serum S100B levels than the nonresponders.Conclusion
The results of this study suggest that the baseline serum S100B level is associated with the subsequent response to antidepressants. In addition, the high baseline serum S100B level that was observed in depressive patients may enhance neuroplasticity, which results in a favorable therapeutic response to antidepressants. 相似文献18.
P.J.W. Naudé U.L.M. Eisel H.C. Comijs N.A. Groenewold P.P. De Deyn F.J. Bosker P.G.M. Luiten J.A. den Boer R.C. Oude Voshaar 《Journal of psychosomatic research》2013
Objective
Systemic low graded inflammation has been identified as a possible biological pathway in late-life depression. Identification of inflammatory markers and their association with characteristics of depression is essential with the aim to improve diagnosis and therapeutic approaches. This study examines the determinants of plasma Neutrophil Gelatinase-Associated Lipocalin (NGAL), which is selectively triggered by TNFα receptor 1 signaling within the central nervous system, and its association with late-life depressive disorder.Methods
Baseline data were obtained from a well-characterized prospective cohort study of 350 depressed and 129 non-depressed older persons (≥ 60 years). Past 6 month diagnosis of major depressive disorder (MDD) according to DSM-IV-TR criteria was assessed with the Composite International Diagnostic Interview (CIDI 2.0). Potential determinants of plasma NGAL included sociodemographic characteristics, lifestyle and psychiatric and physical comorbidity.Results
Plasma NGAL concentrations were significantly associated with age, male gender, smoking and waist circumference. Adjusted for these determinants, depressed patients had significantly higher NGAL plasma levels compared to non-depressed comparison group. Depressed patients who did not meet full criteria for MDD in the month before sampling (partially remitted) had lower plasma NGAL levels compared with those who did. Subjects with a recurrent depression had higher plasma NGAL levels compared to those with a first episode. NGAL levels were neither related with specific symptom profiles of depression nor with antidepressant drug use.Conclusion
Adjusted for confounders, NGAL plasma levels are increased in depressed older persons, without any effect of antidepressant medication and age of onset. 相似文献19.
Yoshimura R Kishi T Suzuki A Umene-Nakano W Ikenouchi-Sugita A Hori H Otani K Iwata N Nakamura J 《Progress in neuro-psychopharmacology & biological psychiatry》2011,35(4):1022-1025
Background
We investigated the relationship between a brain-derived neurotrophic factor (BDNF) polymorphism (Val66Met) and the clinical response of patients with major depressive disorder to selective serotonin reuptake inhibitors (SSRIs; here, paroxetine and sertraline). In addition, serum BDNF levels in these patients were considered together with the clinical response.Methods
A total of 132 patients who met the DSM-IV criteria for major depressive disorder were enrolled in the study. 54 of these patients were male and 78 were female (age range, 20-74 years; mean ± S.D., 51 ± 15). The patients' clinical improvement was evaluated using the 17-item Hamilton Rating Scale for Depression (HAMD-17) before (T0) and at 8 weeks after the administration of SSRI treatment (T8). Patients with at least a 50% decrease in the HAMD-17 score were classified as responders.Results
No correlation was observed between the BDNF Val66Met polymorphism and response to SSRIs or between the BDNF Val66Met polymorphism and serum BDNF levels at T0. An inverse correlation was found between serum BDNF levels and HAMD-17 scores at T0.Conclusions
These results suggest that the BDNF Val66Met polymorphism is independent of both the response to SSRI treatment and serum BDNF levels. The findings in the present study reconfirm that the serum BDNF level is a state biomarker for depression. 相似文献20.
Georgios Paslakis Peter Luppa Daniel Kopf Florian Lederbogen 《Journal of psychiatric research》2010,44(8):556-560