Serum brain-derived neurotrophic factor levels in conversion disorder: Comparative study with depression

The aim of the present study was to compare serum brain-derived neurotrophic factor (BDNF) levels of patients with major depressive disorder (MDD) and conversion disorder (CD). Serum BDNF levels were measured in the following three groups: 15 CD patients without any comorbid diagnosis of psychiatric disorder, 24 patients with MDD, and 26 healthy subjects without any psychiatric diagnosis or psychiatric treatment. The serum BDNF level of the healthy control group (31.4 +/- 8.8 ng/mL) was statistically higher than the level of the MDD group (21.2 +/- 11.3 ng/mL) and the CD group (24.3 +/- 9.0 ng/mL; P = 0.008). This suggests that BDNF level may play a similar role in the pathophysiology of MDD and CD.     

Serum BDNF levels in suicide attempters related to psychosocial stressors: a comparative study with depression

Although many studies have examined the neurobiological aspects of suicide, the molecular mechanisms and pathophysiologic mechanisms associated with suicide remain unclear. In this study, it is aimed to investigate whether there is a difference in serum brain-derived neurotrophic factor (BDNF) levels among suicide attempters without a major psychiatric disorder, compared to major depressive disorder patients and healthy subjects. It was undertaken with the hypothesis that suicide per se lowers serum BDNF levels, since it is a source of stress. The study was carried out in Celal Bayar University Hospital, Manisa, Turkey. Ten suicide attempters, 24 patients with major depressive disorder and 26 subjects without any psychiatric diagnosis and any psychiatric treatment were included in the study. All subjects were asked to give their written consent. Blood samples were collected at the baseline. Serum BDNF was kept at -70 degrees C before testing, and assayed with an ELISA kit (Promega; Madison, Wisc., USA) after dilution with the block and sample solution provided with the kit. The data were subjected to the Kruskal-Wallis test for nonparametric analysis of variance. Mean serum BDNF levels were significantly lower in the suicide group (21.2 +/- 12.4 ng/ml) and the major depressive disorder group (21.2 +/- 11.3 ng/ml) than the control group (31.4 +/- 8.8 ng/ml; p = 0.004). These results suggest that BDNF may play an important role in the neurobiology of suicidal behavior. BDNF levels may be a biological marker for suicidal behavior. To investigate the role of BDNF in suicide, further studies with a wider sample size and a variety of psychiatric diagnoses accompanying suicide attempt are needed.     

The effect of chronic antidepressant treatment on serum brain-derived neurotrophic factor levels in depressed patients: a preliminary study

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.     

Alterations of serum levels of brain-derived neurotrophic factor (BDNF) in depressed patients with or without antidepressants.

BACKGROUND: Because researchers have reported that antidepressants increase the expression of brain-derived neurotrophic factor (BDNF) in the rat hippocampus, we investigated whether serum BDNF levels may be used as a putative biological marker for major depressive disorders (MDD). METHODS: We measured serum BDNF in the following three groups: antidepressant-naive patients with MDD (n = 16), antidepressant-treated patients with MDD (n = 17), and normal control subjects (n = 50). Patients were evaluated using the Hamilton Rating Scale for Depression (HAM-D). Serum BDNF was assayed with the sandwich ELISA method. RESULTS: We found that serum BDNF was significantly lower in the antidepressant-naive group (mean, 17.6 ng/mL; SD, 9.6) than in the treated (mean, 30.6 ng/mL; SD, 12.3; p =.001) or in the control group (mean, 27.7 ng/mL; SD, 11.4; p =.002). There was a significant negative correlation (r = -.350, z = -2.003, p =.045) between serum BDNF and HAM-D scores in all patients. In a preliminary examination, reduced BDNF values of three drug-naive patients recovered to basal levels after antidepressant treatment. CONCLUSIONS: Our study suggests that low BDNF levels may play a pivotal role in the pathophysiology of MDD and that antidepressants may increase BDNF in depressed patients.     

No change between the serum brain-derived neurotrophic factor in female patients with anorexia nervosa before and after partial weight recovery

BACKGROUND: Brain-derived neurotrophic factor (BDNF) is a member of the nerve growth factor family. Several lines of evidence indicate that BDNF plays a role in the pathophysiology of eating disorders (ED). We found that serum BDNF levels in patients with ED were significantly lower than in normal controls. The aim of this longitudinal study was to compare serum BDNF levels in patients with anorexia nervosa (AN) before (n=13, initial mean body mass index (BMI)=14.2 kg/m(2)+/-0.7) and after partial recovery (mean BMI=16.2 kg/m(2)+/-1.7, mean weight gain 5.0 kg+/-2.0), with age-matched normal control subjects (n=17, mean BMI=20.4 kg/m(2)+/-1.5). METHODS: Eating related psychopathology and depressive symptoms were evaluated before and after partial weight recovery, using the Eating Disorder Inventory-2 (EDI-2) and the 17-item Hamilton Depression Rating Scale (HDRS). Serum BDNF levels were measured using a sandwich enzyme-linked immunosorbent assay. RESULTS: Serum BDNF levels with the AN patients (14.5+/-4.4 ng/ml) were significantly (p<0.01) lower than in control subjects (22.1+/-8.9 ng/ml). There were no significant differences in serum BDNF levels between the patients with AN before (14.5+/-4.4 ng/ml) and after (17.2+/-6.9 ng/ml) partial weight recovery. In all subjects, there was a positive correlation (r=0.5, p<0.01) between the baseline BDNF levels and the EDI-2 scores (n=30). Furthermore, in all subjects there was a positive correlation (r=0.4, p<0.05) between the BDNF levels and the BMI. CONCLUSIONS: Serum BDNF levels did not change after partial weight recovery in AN patients. Our results suggest that an alteration of the serum BDNF in AN patients is not due to changes in body weight. Thus, other possible mechanisms that could be related to low serum BDNF levels in AN patients should be evaluated.     

Reduced serum levels of brain-derived neurotrophic factor in adult male patients with autism

BACKGROUND: The precise mechanisms underlying the pathophysiology of autism are currently unknown. Given the key role of brain-derived neurotrophic factor (BDNF) in brain development, we hypothesized that BDNF may play a role in the pathophysiology of autism. In this study, we studied whether serum levels of BDNF are altered in patients with autism. METHODS: We measured serum levels of BDNF in 18 adult male patients with autism and 18 age-matched healthy male control subjects. RESULTS: The serum levels of BDNF in patients with autism (25.6+/-2.15 ng/ml (mean+/-S.D.)) were significantly (z = -4.42, p < 0.001) lower than those of normal controls (61.6+/-10.9 ng/ml (mean+/-S.D.)). Nevertheless, we found no correlations between BDNF levels and clinical variables in autistic patients. CONCLUSIONS: This study suggests that reduced BDNF levels may play a role in the pathophysiology of autism.     

抑郁症患者脑源性神经营养因子Val66Met多态性与血清浓度的关系

目的探讨脑源性神经营养因子（BDNF）基因Val66Met多态性与抑郁症之同的关系以及Val66Met多态性是否影响血清BDNF浓度。方法对76例未经药物治疗的抑郁症患者和50例正常人,用限制性片段长度多态性方法分析Val66Met多态性,采用酶联吸附反应方法对血清BDNF浓度进行检测。结果（1）抑郁症患者血清BDNF浓度（24．7±12．7）ng／m1显著低于正常对照组（36．6±16．4）pg／m｜,差异有统计学意义（P〈0．01）;（2）抑郁症组和对照组之间的Val66Met多态性位点的等位基因频率和基因型分布差异无统计学意义（P〉0．05）;（3）在抑郁症组和对照组,Val／Met＋Met／Met基因型组与Val／Val基因型相比,血清BDNF浓度差异无统计学意义（P〉0．05）。结论抑郁症患者存在较低的血清BDNF水平,BDNF基因Val66Met多态性与抑郁症之间无相关性,Val66Met多态性对血清BDNF水平浓度无明显影响。     

Low plasma BDNF is associated with suicidal behavior in major depression

Brain-derived neurotrophic factor (BDNF), the most abundant neurotrophin in the brain, has a known association with the pathophysiology of anxiety and depression. However, the role of BDNF in suicide has not been well investigated to date. This study examined plasma BDNF levels in 32 major depressive disorder (MDD) patients who had recently attempted suicide, 32 non-suicidal MDD patients, and 30 normal controls. The lethality of the suicide attempt was measured using the Risk-Rescue Rating (RRR) and Lethality Suicide Attempt Rating Scale (LSARS). The severity of depression was measured with the Hamilton Depression Rating Scale (HDRS). Plasma BDNF levels were measured by enzyme linked immunosorbent assay. BDNF levels were significantly lower in suicidal MDD patients (430.5+/-397.0 pg/ml) than non-suicidal MDD patients (875.80+/-663.02 pg/ml) or normal controls (889.4+/-611.3 pg/ml) (F=6.682, p=0.002). The most suitable cut-off point of BDNF level between suicidal depression and non-suicidal depression groups was 444.58 pg/ml. At this cut-off point, the sensitivity=68.7%, specificity=78.1%, positive predictive value=75.9%, and negative predictive value=71.4%. However, there was no significant difference in BDNF levels between the depressive control and normal control groups (p=0.996). LSARS and RRR did not reveal any significant correlations with BDNF levels in suicidal patients. In addition, BDNF levels were not different between fatal and non-fatal suicide attempts. These results suggest that reduction of plasma BDNF level is related to suicidal behavior in major depression and that BDNF level may be a biological marker of suicidal depression.     

Plasma brain-derived neurotrophic factor as a peripheral marker for the action mechanism of antidepressants

Numerous studies have demonstrated that depression is associated with a decreased expression of brain-derived neurotrophic factor (BDNF). BDNF shows antidepressant-like effects in animal models. Therefore, we tested the hypothesis that BDNF might be a peripheral marker for the mechanism of action of antidepressant agents in humans. Thirty-two patients meeting the DSM-IV criteria for major depressive disorder and 50 normal control subjects were recruited for this study. Plasma BDNF levels and Hamilton Depression Rating Scales were measured at baseline and 6 weeks after antidepressant administration. At baseline, the mean plasma BDNF level was lower in the depressive patients (698.1 +/- 537.7 pg/ml) than in the control subjects (830.7 +/- 624.8 pg/ml), although the difference was not statistically significant (p = 0.33). The plasma BDNF levels in depressive patients significantly increased from 698.1 +/- 537.7 to 1,028.9 +/- 744.5 after 6 weeks of antidepressant treatment (p = 0.01). Moreover, plasma BDNF levels were significantly increased after 6 weeks of treatment in the responder group, while there was no statistically significant change in the unresponsive group. These results suggest that the therapeutic response after antidepressant administration might be attributable to the increase in BDNF levels. BDNF may play a critical role in the action mechanism of antidepressant drugs. Further studies with a larger number of subjects are needed to verify these findings.     

Effects of tryptophan depletion on serum levels of brain-derived neurotrophic factor in unmedicated patients with remitted depression and healthy subjects

OBJECTIVE: Data suggest the involvement of serotonergic and neurotrophic systems in major depressive disorder. To investigate their potential interaction, the authors studied changes in serum levels of brain-derived neurotrophic factor (BDNF) during tryptophan depletion and sham depletion in unmedicated patients with remitted major depressive disorder and in a group of healthy comparison subjects. METHOD: Twenty-seven patients with remitted major depressive disorder and 20 healthy subjects underwent tryptophan depletion and sham depletion in a randomized, placebo-controlled, double-blind crossover study. Serum BDNF concentrations and plasma tryptophan concentrations as well as behavioral assessments were obtained. RESULTS: During tryptophan depletion, BDNF levels increased in healthy volunteers. By contrast, patients with remitted major depressive disorder were unable to mount this presumed compensatory response, and BDNF levels remained low in these patients. CONCLUSIONS: The results further substantiate the potential role of BDNF in major depressive disorder.     

Decreased levels of serum brain-derived neurotrophic factor in both depressed and euthymic patients with unipolar depression and in euthymic patients with bipolar I and II disorders

OBJECTIVES: Brain-derived neurotrophic factor (BDNF) has been proposed as a candidate molecule in the pathophysiology of major depressive disorder (MDD) and bipolar disorders (BD). Reduced levels of peripheral BDNF have been found in drug-free MDD patients, in drug-treated depressed or manic patients with BD type I (BD-I), but not in drug-treated euthymic BD-I individuals. No study has been done in patients with BD type II (BD-II). Moreover, the influence of Axis I psychiatric comorbidity on circulating BDNF in affective patients has never been evaluated. Therefore, in the present study, we aimed: (i) to confirm previous findings on peripheral BDNF in MDD and BD-I patients; (ii) to assess whether changes in circulating BDNF occur also in patients with BD-II; and (iii) to exclude the possibility that comorbid psychiatric disorders exerted an effect on BDNF levels in affective patients. METHODS: We measured serum BDNF concentrations by an enzyme-linked immunosorbent assay method in 85 subjects, including 24 euthymic patients with unipolar depression (UD), 17 euthymic patients with BD-I, 11 euthymic patients with BD-II, 11 UD patients with a current major depressive episode and 22 drug-free healthy controls. At the time of the study, 15 patients were drug-treated; the remaining ones were drug-free for at least four weeks. RESULTS: Compared to healthy controls, serum BDNF concentrations were significantly reduced in all the patient groups (F(4,80) = 3.840, p = 0.006) with no significant difference among them. Drug treatments and comorbid psychiatric disorders had no effect on lowered circulating BDNF levels in affective patients. CONCLUSIONS: Present results confirm previous independent findings of reduced circulating BDNF in patients with MDD and report, for the first time, decreased serum BDNF levels in euthymic patients with UD, BD-I and BD-II, independently from drug treatment status and concomitant Axis I psychiatric disorders.     

Open-label evaluation of venlafaxine sustained release in outpatients with generalized anxiety disorder with comorbid major depression or dysthymia: effectiveness,tolerability and predictors of response

In a setting of routine clinical practice, 32 outpatients with generalized anxiety disorder (GAD) and major depression (MD) (n = 21) or dysthymia (n = 11), according to DSM-IV criteria, were consecutively treated with flexible dosages of sustained-release venlafaxine (SR-VF) for at least 8 weeks. In a 16-week follow-up, SR-VF daily dose could be modified on the basis of the therapeutic response and of the side effect profile. Symptomatological modifications were explored by means of the Clinical Global Impression (CGI) scale, Hamilton Rating Scale for Depression (HAM-D), and Hamilton Anxiety Scale (HAM-A). SR-VF was well tolerated and only 2 patients interrupted the treatment before 24 weeks; the mean final dose +/- SD was 135.5 +/- 71.8 mg (range 75-225); in 26 (81.2%) patients, a statistically significant response was observed in depressive symptomatology within the first 8 weeks. The mean total score of HAM-D showed a significant reduction during the first 8 weeks of treatment, while the mean total score of HAM-A did not present a significant reduction until week 24. In patients with MD, a statistically significant response was observed after the first 8 weeks, while the reduction of the anxiety scores required more time and, in some cases, did not appear at all. Conversely, in patients with GAD and dysthymia, anxious and depressive symptomatology improved simultaneously. Stepwise multiple regression indicated that the improvement of depression is negatively related to a high score of CGI anxiety severity, and the improvement of anxiety is related to the presence of dysthymia and, to a lesser extent, to a short duration of the illness. Our data confirm the effectiveness and tolerability of SR-VF in mixed anxiety-depressive states. The differential response suggests a pathophysiologic and clinical distinction between GAD with comorbid MD or dysthymia.     

Evidence for a relationship between genetic variants at the brain-derived neurotrophic factor (BDNF) locus and major depression.

BACKGROUND: Previous genetic studies investigating a possible involvement of variations at the brain derived neurotrophic factor (BDNF) gene locus in major depressive disorder (MDD), bipolar affective disorder (BPAD), and schizophrenia have provided inconsistent results. METHODS: We performed single-marker and haplotype analyses using three BDNF polymorphisms in 2,376 individuals (465 MDD, 281 BPAD, 533 schizophrenia, and 1,097 control subjects). RESULTS: Single-marker analysis did not provide strong evidence for association. Haplotype analysis of marker combination rs988748-(GT)n-rs6265 produced nominally significant associations for all investigated phenotypes (global p values: MDD p = .00006, BPAD p = .0057, schizophrenia p = .016). Association with MDD was the most robust finding and could be replicated in a second German sample of MDD patients and control subjects (p = .0092, uncorrected). Stratification of our schizophrenia sample according to the presence or absence of a lifetime history of depressive symptoms showed that our finding in schizophrenia might be attributable mainly to the presence of depressive symptoms. CONCLUSIONS: Association studies of genetic variants of the BDNF gene with various psychiatric disorders have been published with reports of associations and nonreplications. Our findings suggest that BDNF may be a susceptibility gene for MDD and schizophrenia-in particular, in a subgroup of patients with schizophrenia with a lifetime history of depressive symptoms.     

Mental disorder in youth suicide. DSM-III-R Axes I and II

A 3-year urban material of suicides in adolescents and young adults (age 15-29 years) was studied retrospectively by means of interviews with survivors (n = 58). Classification of mental disorders according to DSM-III-R showed that major depression was important as background to suicides in 41%, primary (22%) or secondary (19%) to other disorders. Adding major depression, depressive disorder, not otherwise specified, dysthymia and adjustment disorder with depressed mood gave a total of 64% depressive syndromes. Schizophrenia (14%) and borderline personality disorder (28%) constituted other relevant groups. Coexisting substance use disorder occurred in 47%. A majority of the subjects (72%) were known by psychiatric caregivers and 16% committed suicide during inpatient care.     

A double-blind comparison study of nomifensine and imipramine in treating depressed patients

Nomifensine was compared to imipramine in treatment of 40 patients with endogenous major depressive disorder. After one week washout, patients were randomly assigned to 5 weeks treatment with Nomifensine or Imipramine. Mean scores for HAM-D, HAM-A, GAS were significantly improved in both treatment groups (P less than 0.01). Two agents were similar in antidepressant efficacy and rapidity of action. Nomifensine treatment group had fewer side effect, whereas the Imipramine group had more adverse experiences. Effects of Nomifensine on the ECG were compared to those of imipramine. Both drugs increased heart rate. Nomifensine less than imipramine. QT measurement interval revealed a statistically significant decrease in imipramine group. Plasma Nomifensine and imipramine concentrations were not correlated with clinical response, side effects or electrocardiographic parameters. The steady-state plasma concentration 105 +/- 47ng/ml for nomifensine, 860 +/- 773ng/ml for imipramine were offaimed respectively at the fixed dose (225mg/day) during the 35 treatment day.     

Serum brain-derived neurotrophic factor (BDNF) levels in patients with panic disorder: as a biological predictor of response to group cognitive behavioral therapy

Little is known about biological predictors of treatment response in panic disorder. Our previous studies show that the brain-derived neurotrophic factor (BDNF) may play a role in the pathophysiology of major depressive disorders and eating disorders. Assuming that BDNF may be implicated in the putative common etiologies of depression and anxiety, the authors examined serum BDNF levels of the patients with panic disorder, and its correlation with therapeutic response to group cognitive behavioral therapy (CBT). Group CBT (10 consecutive 1 h weekly sessions) was administered to the patients with panic disorder after consulting the panic outpatient special service. Before treatment, serum concentrations of BDNF and total cholesterol were measured. After treatment, we defined response to therapy as a 40% reduction from baseline on Panic Disorder Severity Scale (PDSS) score as described by [Barlow, D.H., Gorman, J.M., Shear, M.K., Woods, S.W., 2000. Cognitive-behavioral therapy, imipramine, or their combination for panic disorder: A randomized controlled trial. JAMA. 283, 2529-2536]. There were 26 good responders and 16 poor responders. 31 age- and sex-matched healthy normal control subjects were also recruited in this study. The serum BDNF levels of the patients with poor response (25.9 ng/ml [S.D. 8.7]) were significantly lower than those of the patients with good response (33.7 ng/ml [S.D. 7.5]). However, there were no significant differences in both groups of the patients, compared to the normal controls (29.1 ng/ml [S.D. 7.1]). No significant differences of other variables including total cholesterol levels before treatment were detected between good responders and poor responders. These results suggested that BDNF might contribute to therapeutic response of panic disorder. A potential link between an increased risk of secondary depression and BDNF remains to be investigated in the future.     

Serum brain-derived neurotrophic factor levels as a novel biological marker for the activities of psychiatric symptoms in systemic lupus erythematosus

Abstract

Objectives. Neuropsychiatric systemic lupus erythematosus (NPSLE) is a serious but potentially treatable disease. However, biological markers such as IgG index or IL-6 do not always reflect the severity of the psychotic symptoms of NPSLE. We hypothesized that serum BDNF levels may be a biological marker for reflecting the severity of the psychiatric symptoms of NPSLE. Methods. The participants enrolled in this study were 28 healthy volunteers and 54 Japanese SLE inpatients at the University Hospital of Occupational and Environmental Health, all of whom fulfilled the criteria for the classification of SLE. SLE patients were divided into the three groups: NPSLE with psychiatric symptoms including an acute confusional state, anxiety disorder, cognitive dysfunction, mood disorder, and psychosis (NP group); NPSLE without psychiatric symptoms (NN group); and SLE without neuropsychiatric symptoms (S group). The serum BDNF levels were measured by ELISA. Results. Serum BDNF levels were significantly increased in the NP group (mean ± SE = 37.0 ± 5.46 ng/ml) compared with those in the other three groups (NN group; mean ± SE=9.1 ± 2.44 ng/ml, P < 0.0001, S group; mean ± SE=10.4 ± 2.51 ng/ml, P < 0.0001, healthy control; mean ± SE= 11.44 ± 0.69, P < 0.0001). Subsequently, serum BDNF levels were decreased in parallel with the improvement of psychiatric symptoms in the NP group. Conclusion. These results suggest that serum BDNF is a biological marker for the severity of psychiatric symptoms in NPSLE patients.     

Pharmacotherapy plus psychotherapy for treatment of depression in active injection drug users

CONTEXT: Depressive disorders are common among opiate abusers and are associated with detrimental behavioral effects. However, there is little precedent for offering active drug users complex treatments for depression. OBJECTIVE: To determine whether combined psychotherapy and pharmacotherapy treatment reduces reported depressive symptoms compared with an assessment-only condition among out-of-treatment drug injectors. DESIGN: Randomized controlled trial. SETTING: Research office located at an academic medical center. PATIENTS: Active injection drug users with a DSM-IV diagnosis of major depression, dysthymia, substance-induced mood disorder with symptoms persisting for at least 3 months, or major depression plus dysthymia, and a Modified Hamilton Rating Scale for Depression (HAM-D) score greater than 13. INTERVENTION: Combined psychotherapy (8 sessions of cognitive behavior therapy) plus pharmacotherapy (citalopram). MAIN OUTCOME MEASURES: Modified HAM-D scale scores at the end of 3 months of combined treatment. RESULTS: The 109 study subjects were 64% male and had a mean age of 36.7 years and a mean baseline HAM-D score of 20.7. Depression subtypes included major depression only (63%), substance-induced depression (17%), and major depression plus dysthymia (17%). In the intent-to-treat analysis, participants in treatment averaged 2.11 HAM-D points greater improvement than control subjects (P=.08), and 26.1% of combined treatment patients (n=53) compared with 12.5% of control patients (n=56) were in remission (P=.047). Nearly 40% of fully adherent subjects (receiving >75% of either psychotherapy or pharmacotherapy) were in remission at follow-up (odds ratio, 3.6; P=.04). CONCLUSIONS: Combined treatment for depression is significantly superior to a control condition (assessment only) in proportion of patients in remission, but not in HAM-D improvement among drug injectors. Full adherence to treatment is associated with the largest treatment effects. Our findings demonstrate that active drug users with dual diagnoses are able to participate in conventional treatment.     

Carotid intima-media thickness in late-onset major depressive disorder

BACKGROUND: This study explored whether patients with late-onset major depressive disorder showed higher carotid artery intima-medium thickness (IMT) and investigated the relationship between the IMT and white matter hyperintensities on magnetic resonance imaging (MRI) among patients. METHODS: Fourteen elderly patients with late-onset major depressive disorder from a psychiatric outpatient clinic and 11 non-depressed controls received a comprehensive psychiatric assessment, ultrasound IMT measurements of the carotid arteries, and cerebral MRI. RESULTS: The carotid IMT was higher in the patient group vs the control group (1.26 +/- 0.30 vs 1.00 +/- 0.20 mm; t = 2.40, p < 0.03). The difference was more apparent in the common carotid artery (1.20 +/- 0.32 vs 0.97 +/- 0.13 mm; t = 2.31, p < 0.04). There was a high correlation (r = 0.55, p < 0.05) between the carotid IMT and white matter hyperintensities among patients with late-onset major depressive disorder. CONCLUSION: Results of this study suggest that atherosclerosis represented by the carotid IMT contributes to the development of late-onset major depressive disorder. The findings support the vascular depression hypothesis.     

Measurements of brain-derived neurotrophic factor: methodological aspects and demographical data

Although numerous studies have dealt with changes in blood brain-derived neurotrophic factor (BDNF), methodological issues about BDNF measurements have only been incompletely resolved. We validated BDNF ELISA with respect to accuracy, reproducibility and the effect of storage and repeated freezing cycles on BDNF concentrations. Additionally, the effect of demographic characteristics in healthy subjects on BDNF was verified. Whole blood and serum was collected from 206 healthy subjects and a subgroup was genotyped for BDNF Val66Met polymorphism. The effect of age, gender, BDNF genotype and thrombocyte count on whole blood BDNF was assessed. The BDNF ELISA measurement was accurate, 91.6+/-3.0%, and showed high reproducibility, whereas inter-assay and intra-subject variations were modest, 8.4+/-5.2% and 17.5+/-14.1%, respectively. Storage of whole blood samples at 4 degrees C significantly decreased BDNF concentration, while repeated freezing cycles and storage at -20 degrees C was without any effect. Storage at -20 degrees C of serum, but not whole blood, was associated with a significant decrease in BDNF concentration. Women had significantly higher whole blood BDNF concentrations than men (18.6+/-1.3 ng/ml versus 16.5+/-1.4 ng/ml), and showed a right-skewed BDNF concentration distribution. No association between whole blood BDNF concentrations and thrombocyte count, age, or BDNF genotype was found. In conclusion, the BDNF ELISA assay determines whole blood BDNF accurately and with high reproducibility. Female gender is associated with higher whole blood BDNF concentrations whereas age, thrombocyte count and BDNF Val66Met polymorphism were un-associated.