***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: INTRODUCTION Depression , stress and antidepressant treatment have been found to modulate the expression of brain-derived neurotrophic factor ( BDNF ) . Recent research suggests that serum BDNF concentration is reduced in depression and that antidepressant treatment leads to an increase in serum BDNF concentration . METHODS We studied depressed patients receiving a r and omized antidepressant treatment with either mirtazapine ( n=29 ) or venlafaxine ( n=27 ) for 28 days in a prospect i ve design . Changes in the concentrations of serum neurotrophins in response to antidepressant treatment were assessed . RESULTS There was a significant " treatment " by " medication " interaction effect on BDNF serum concentrations that indicated a decline of BDNF in venlafaxine-treated patients ( 7.82±3.75 - 7.18±5.64 ng/mL ) , while there was an increase in mirtazapine-treated patients ( 7.64±6.23 - 8.50±5.37 ng/mL ) . There was a trend for a " treatment " by " remission " interaction with a favourable clinical course being related to increasing serum BDNF . DISCUSSION Changes in BDNF serum concentrations as a result of antidepressant therapy depend on the antidepressant and potentially on the clinical course 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 Electroconvulsive therapy ( ECT ) is effective for patients with antidepressant medication-resistant depression . However , the mechanisms of ECT 's effectiveness for treating depression are not fully understood . We therefore investigated ECT 's effects on blood levels of brain-derived neurotrophic factor ( BDNF ) , catecholamine metabolites , and nitric oxide ( NO ) in 18 treatment-refractory depressed patients .  Serum BDNF levels increased significantly following ECT in responders to ECT ( before ECT : 8.0+/-9.7 ng/mL ; five weeks after start of ECT : 15.1+/-11.1 ng/mL ) , whereas BDNF levels in non-responders were unchanged ( before ECT : 11.5+/-11.0 ng/mL ; five weeks after start of ECT : 9.4+/-7.5 ng/mL ) . Furthermore , the plasma HVA levels , but not MHPG levels , were significantly reduced after ECT ( before ECT : 8.5+/-1.9 ng/mL ; five weeks after start of ECT : 5.8+/-2.2 ng/mL ) . This latter finding occurred in parallel with the improvement of depressive symptoms in all patients . These results suggest that the mechanisms underlying ECT 's effect on refractory depression may be related to dopaminergic neurons and BDNF Objective : Brain-derived neurotrophic factor ( BDNF ) levels are decreased in individuals with depression and increase following antidepressant treatment . The objective of this study is to compare pre- and post-treatment serum BDNF levels in patients with drug-resistant major depressive disorder ( MDD ) who received either electroconvulsive therapy ( ECT ) or repetitive transcranial magnetic stimulation ( rTMS ) .  It is hypothesized that non-pharmacological treatments also increase serum BDNF levels . Methods : This was a prospect i ve , single-blind study comparing pre- and post-treatment serum BDNF levels of 29 patients with drug-resistant MDD who received ECT or rTMS treatment .  Serum BDNF levels were measured 1 week prior to and 1 week after treatment using the s and wich ELISA technique . Depression severity was measured 1 week before and 1 week after treatment using the Hamilton Depression Rating Scale . Two-sided normal distribution paired t-test analysis was used to compare pre- and post-treatment BDNF concentration and illness severity . Bivariate correlations using Pearson ’s coefficient assessed the relationship between post-treatment BDNF levels and post-treatment depression severity . Results : There was no significant difference in serum BDNF levels before and after ECT , although concentrations tended to increase from a baseline mean of 9.95–12.29 ng/ml after treatment ( p = 0.137 ) . Treatment with rTMS did not significantly alter BDNF concentrations ( p = 0.282 ) . Depression severity significantly decreased following both ECT ( p = 0.003 ) and rTMS ( p < 0.001 ) . Post-treatment BDNF concentration was not significantly correlated with post-treatment depression severity in patients who received either ECT ( r = −0.133 , p = 0.697 ) or rTMS ( r = 0.374 , p = 0.126 ) . It is important to note that these results are based on the small number of patients included in this study . Conclusion : This study suggests that ECT and rTMS may not exert their clinical effects by altering serum BDNF levels in patients with drug-resistant MDD .  Serum BDNF concentration may not be a biomarker of ECT or rTMS treatment response Several findings have suggested that the neurotrophin BDNF could contribute to clinical efficacy of antidepressant treatments . The purpose of this study was to analyse if ECT operates a modulation of serum BDNF levels in a sample of drug resistant depressed patients . The results obtained show significantly higher serum levels of BDNF following ECT . More specifically , while no change occurred in the whole sample between T0 ( baseline ) and T1 ( after ECT ) ( p=0.543 ) a significant increase has been identified at T2 , one month after the end of ECT ( p=0.002 ) . However , the BDNF augmentation was evident even between T0 and T1 in a subgroup of patients who has low baseline BDNF levels . Although future research es are needed , the results herein presented show for the first time that ECT is associated with changes in serum BDNF and further support the possible involvement of BDNF in antidepressant therapies G*Power is a free power analysis program for a variety of statistical tests . We present extensions and improvements of the version introduced by Faul , Erdfelder , Lang , and Buchner ( 2007 ) in the domain of correlation and regression analyses . In the new version , we have added procedures to analyze the power of tests based on ( 1 ) single- sample tetrachoric correlations , ( 2 ) comparisons of dependent correlations , ( 3 ) bivariate linear regression , ( 4 ) multiple linear regression based on the r and om predictor model , ( 5 ) logistic regression  , and ( 6 ) Poisson regression . We describe these new features and provide a brief introduction to their scope and h and ling INTRODUCTION Stress , glucocorticoids and anti-depressant treatment have been found to modulate the expression of brain-derived neurotrophic factor ( BDNF ) and nerve growth factor ( NGF ) . Recent research suggests that serum BDNF concentration is reduced in depression and that successful antidepressant treatment leads to an increase in serum BDNF concentration . METHODS We studied depressed patients receiving a st and ardized antidepressant treatment with either 150 mg amitriptyline ( n=20 ) or 40 mg paroxetine ( n=20 ) for 36 days in a prospect i ve design . Changes in the concentrations of serum neurotrophins and salivary cortisol in response to antidepressant treatment were assessed . RESULTS Independent of clinical efficacy there was a significant ' treatment ' by ' medication ' interaction effect on BDNF serum concentrations that indicated a decline of BDNF by 12 % in paroxetine-treated patients while there was an increase by 13 % in amitriptyline-treated patients . Neither antidepressant altered NGF concentrations . The changes in cortisol and neurotrophin concentrations were not related . DISCUSSION Changes in BDNF serum concentrations as a result of antidepressant therapy depend on the antidepressant instead of being a general characteristic of response to antidepressant treatment Brain-derived neurotrophic factor ( BDNF ) is an important member of the neurotrophin family of growth factors , abundant in the brain and periphery . Research ers have reported that serum BDNF levels in drug-free depressed patients are lower than those of healthy controls , and have proposed that these low levels might reflect a failure of neuronal plasticity in depression . In the present study , we investigated the effects of paroxetine , an SSRI , and milnacipran , an SNRI , on serum BDNF levels in depressed patients .  Serum levels of BDNF were measured by ELISA before , 4 weeks , and 8 weeks after the start of treatment with antidepressants . Forty-two patients were r and omly administered  paroxetine ( 21 cases ) or milnacipran ( 21 cases ) . A negative correlation was found between serum BDNF levels and baseline Ham-D scores . The response and remission rates for each drug were not significantly different . Serum BDNF levels in responders were significantly increased 2.6- and 1.8-fold 8 weeks after treatment with paroxetine or milnacipran , respectively . These results suggest that both drugs improve the depressive state by increasing BDNF levels There is accumulating evidence that a deficiency in brain-derived neurotrophic factor ( BDNF ) plays a critical role in the pathophysiology of depression . This is in line with the postulate that low BDNF levels in serum are associated with depression . However , the regulation of maternal BDNF serum levels in the perinatal period , and its relationship to maternal depression is unknown . In this study ,  serum BDNF concentrations  were measured in 40 pregnant ( follow-up : 30th and 37th week of gestation , 1 week and 8 weeks after childbirth ) and 40 non-pregnant women ( 20 - 40 years old ) . The  Edinburgh Postnatal Depression Scale ( EPDS ) was assessed in all subjects at all time points . Maternal serum levels of BDNF were markedly decreased , both before and after childbirth ( median : < 30 % of non-pregnant controls ) . BDNF correlated with decreased Serotonin ( 5-HT ) levels in serum ( r>0.6 and p<0.001 at all time points ) . In contrast , there was no association with altered estrogen , progesterone , dehydroepi and rosterone or cortisol concentrations in serum . There were significantly higher cortisol levels in cases of maternal depression ( EPDS scores>9 points ) than in cases without depression . There was a trend to a decrease of BDNF and 5-HT levels in cases of maternal depression ( as compared to cases without depression ) , but this was not significant . In conclusion , we demonstrate that women display markedly decreased BDNF serum levels before and after childbirth . This phenomenon might reflect an increased risk for the development of mood disorders in the perinatal period . However , the individual serum concentration of BDNF alone did not predict maternal depression in our study BACKGROUND Brain Derived Neurotrophic Factor ( BDNF ) has potential as a biomarker of depression treatment because serum BDNF in depressed human subjects is decreased and normalizes with treatment . The relationship between serum BDNF and exercise treatment of depression is not known . The Treatment with Exercise Augmentation for Depression ( TREAD ) study examined dosed exercise augmentation treatment of partial responders to antidepressants . Serum BDNF in TREAD subjects was analyzed to underst and its relationship with exercise training . METHODS Subjects were r and omized to  high ( 16 kcal/kg/week or KKW ) or low ( 4 KKW ) energy expenditure exercise  over 12 weeks . Actual kcal/week expended and IDS-C scores were collected weekly . One hundred four subjects in TREAD provided baseline blood sample s ; a subset of 70 subjects also provided week  
    Output:
    
Meta-analyses , published in 2008–2010 , have confirmed abnormally low serum brain-derived neurotrophic factor ( BDNF ) concentrations in depressed patients and normalization of this by antidepressant treatment .
Finally , the aggregated data negate consistent associations between serum BDNF concentrations and the symptom severity of depression .
Our findings corroborate the cl aim that altered serum BDNF concentrations are peripheral manifestations of depression .