***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 
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    Input: 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 After initial interviews with 20,291 adults in the National Institute of Mental Health Epidemiologic Catchment Area Program , we estimated prospect i ve 1-year prevalence and service use rates of mental and addictive disorders in the US population . An annual prevalence rate of 28.1 % was found for these disorders , composed of a 1-month point prevalence of 15.7 % ( at wave 1 ) and a 1-year incidence of new or recurrent disorders identified in 12.3 % of the population at wave 2 . During the 1-year follow-up period , 6.6 % of the total sample developed one or more new disorders after being assessed as having no previous lifetime diagnosis at wave 1 . An additional 5.7 % of the population , with a history of some previous disorder at wave 1 , had an acute relapse or suffered from a new disorder in 1 year . Irrespective of diagnosis , 14.7 % of the US population in 1 year reported use of services in one or more component sectors of the de facto US mental and addictive service system . With some overlap between sectors , specialists in mental and addictive disorders provided treatment to 5.9 % of the US population , 6.4 % sought such services from general medical physicians , 3.0 % sought these services from other human service professionals , and 4.1 % turned to the voluntary support sector for such care . Of those persons with any disorder , only 28.5 % ( 8.0 per 100 population ) sought  mental health/addictive services .  Persons with specific disorders varied in the proportion who used services , from a high of more than 60 % for somatization , schizophrenia , and bipolar disorders to a low of less than 25 % for addictive disorders and severe cognitive impairment . Applications of these descriptive data to US health care system reform options are considered in the context of other variables that will determine national health policy Background Neuroplastic processes are thought to be involved in the pathophysiology of major depression . It has been reported that serum brain-derived neurotrophic factor ( BDNF ) is decreased in depressed patients . Objectives Compare BDNF levels in depressed patients and healthy controls in platelet poor plasma and in washed platelets . Observe the effects of 8- and 24-week treatment with S-citalopram on these levels . Methods We assessed the levels of BDNF in platelet poor plasma and in washed platelets from 18 major depression patients , and compared them with 14 healthy controls . Blood sample s were obtained from patients before and during treatment ( 8 and 24 weeks ) with a  selective serotonin reuptake inhibitor , S-citalopram . Results A significant decrease in severity of depressive symptoms was observed from the first month of treatment with S-citalopram , and symptoms continued decreasing until the 6th month . Plasma BDNF levels in untreated patients appeared significantly increased ( p < 0.01 ) but reached values similar to those of controls at the 24th week . In contrast , levels of platelet BDNF appeared significantly decreased ( p < 0.05 ) , but treatment also normalized levels so that values obtained were equivalent to those of controls . Conclusions Untreated depressed patients showed increased plasma BDNF levels and decreased platelet BDNF levels , as compared with control subjects , and tend to normalize during treatment with S-citalopram for 24 weeks , with BDNF reaching levels similar to those in healthy controls at the 24th week in both sample s. We observed that improvement in depressive symptoms was accompanied by normalization of plasma and platelet BDNF levels 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 Brain-derived neurotrophic factor ( BDNF ) is a c and i date molecule for influencing the clinical response to antidepressant treatment . The aims of this study were to determine the relationship between the Val66Met polymorphism in the BDNF gene and the response to  mirtazapine in 243 Korean subjects with major depressive disorder ( MDD ) . The reduction in the Hamilton Depression score over the 8-week treatment period was not influenced by BDNF V66 M genotypes . A marginal effect of genotype on somatic anxiety score was observed at baseline ( P = 0.047 in the dominant model ) . However , genotype – time interaction had no effect on somatic anxiety score after the 8-week a treatment period . Plasma BDNF levels tended to increase during mirtazapine treatment , although without statistical significance ( P = 0.055 ) . After 8 weeks of mirtazapine  treatment , plasma BDNF levels were higher in Met allele homozygotes ( 1499.7 ± 370.6 ng/mL ) than in Val allele carriers ( 649.7 ± 158.5 ng/mL , P = 0.049 ) . Our results do not support the hypothesis that the Val66Met promoter polymorphism in the BDNF gene influences the therapeutic response  to mirtazapine in Korean MDD patients . However , our data indicate that this polymorphism results in increased plasma BDNF  after mirtazapine treatment 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 sample s 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 In the treatment of patients with major depressive disorder ( MDD ) , early non-improvement of symptoms after initiation of antidepressant treatment is a highly sensitive and specific marker for final treatment failure . On the other h and , meta-analyses of clinical studies investigating serum BDNF ( sBDNF ) concentration before and after antidepressant treatment showed an increase of sBDNF during treatment , which was correlated with amelioration of depressive symptoms . No study has yet investigated the predictive value of early changes of sBDNF for final treatment outcome of the individual patient . The aim of this study was to investigate in patients with MDD , whether i ) the non-increase of sBDNF in the early course of treatment is a specific and sensitive marker for final treatment failure , ii ) whether the sensitivity and specificity of early non-improvement for treatment failure can be increased by combining it with the marker " early non-increase of sBDNF " . For this purpose , we performed a pilot study with 41 in patients with MDD according to DSM-IV , who were treated in a naturalistic setting .  Depression severity and sBDNF were measured in weekly intervals from baseline to week six with the 21-item Hamilton Depression Rating Scale ( HAMD-21 ) and ELISA , respectively . The individual markers sBDNF non-increase and HAMD-21 non-improvement from baseline to day 7 or 14 predicted later non-response and non-remission with moderate to high specificity . The combined marker sBDNF non-increase plus HAMD-21 non-improvement at day 14 increased the specificity for non-response and non-remission to 100 % . Our data provide the first evidence that the absence of an early increase of sBDNF in conjunction with early non-improvement might be a highly specific peripheral marker predictive for treatment failure in patients with MDD . If replicated , this combined marker could be considered useful for prospect i ve confirmatory trials in patients with MDD Brain-derived neurotrophic factor ( BDNF ) and other neurotrophins are believed to play an important role in affective disorders . In this study we investigated plasma-BDNF response during an incremental exercise test in 18 patients suffering from moderate major depressive disorder ( MDD ) and 18 controls . The patients were not treated with antidepressants or neuroleptics . Possible associations between plasma plasma-BDNF levels , dexamethasone suppression test cortisol levels and Montgomery-Asberg Depression Rating Scale ( MADRS ) scores were also tested . No difference in basal BDNF levels between patients and controls was found . BDNF increased significantly during exercise in both male and female patients as well as in male controls , with no significant differences between the groups . BDNF levels declined after exercise , but after 60 min of rest BDNF levels showed tendencies to increase again in male patients . No correlation between BDNF and cortisol or MADRS scores was found . We conclude that unmedicated patients with moderate depression and normal activity of the hypothalamic-pituitary-adrenal axis do not have a disturbed peripheral BDNF release during exercise . The BDNF increase 60 min after interruption of exercise in male patients might indicate up-regulated BDNF synthesis , but this needs to be further investigated in future studies Background : Low brain-derived neurotrophic factor ( BDNF ) levels are observed in both depressed and diabetes patients . Animal research has shown that omega-3 polyunsaturated fatty acids increase BDNF levels . In this exploratory r and omized double-blind placebo-controlled study in diabetes patients with major depression , we tested whether ( a ) omega- 3 ethyl-eicosapentaenoic acid ( 
    Output:
    
However , despite of the methodology , BDNF seems to increase after treatment for major depression