ABSTRACT
Our previous study showed that serum brain-derived neurotrophic factor (BDNF) was significantly decreased in the antidepressant-naive patients with major depressive disorders. However, it was still unclear whether serum BDNF level was altered in drug-naive patients with schizophrenia. Using ELISA, we measured serum BDNF levels in antipsychotic-naive (n=15) and medicated (n=25) patients with schizophrenia, and in age- and sex-matched normal controls (n=40). There were no significant differences in serum BDNF levels among antipsychotic-naive (n=15) and medicated (n=25) patients and normal controls (n=40). Possible factors such as duration of illness, age of onset, Brief Psychiatric Rating Scale scores, and chlorpromazine equivalent dosages of antipsychotics did not reveal any significant correlations with BDNF levels. Our results do not support the view that serum BDNF levels are associated with schizophrenia.
Subject(s)
Brain-Derived Neurotrophic Factor/blood , Brain/metabolism , Brain/physiopathology , Schizophrenia/blood , Adult , Age of Onset , Aged , Antipsychotic Agents/pharmacology , Brain/growth & development , Brain-Derived Neurotrophic Factor/drug effects , Dopamine/metabolism , Dose-Response Relationship, Drug , Female , Humans , Male , Middle Aged , Neurons/metabolism , Schizophrenia/physiopathologyABSTRACT
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.
Subject(s)
Antidepressive Agents/therapeutic use , Brain-Derived Neurotrophic Factor/blood , Depressive Disorder, Major/blood , Depressive Disorder, Major/drug therapy , Adult , Aged , Antidepressive Agents/pharmacology , Biomarkers/blood , Brain-Derived Neurotrophic Factor/drug effects , Case-Control Studies , Enzyme-Linked Immunosorbent Assay , Female , Humans , Male , Middle AgedABSTRACT
Midkine (MK) is a heparin-binding growth factor implicated in various biological phenomena such as development of the hippocampus and anxiety. We evaluated serum MK levels of drug-naive (n=15) and medicated (n=25) patients with schizophrenia, and age- and sex-matched normal controls (n=38). The patients showed two clusters in the levels. Four drug-naive patients (26.7%) and two medicated patients (8.0%) had abnormally high values, but no controls did, there being a significant difference in the numbers (P=0.003, Fisher's exact test). Furthermore, in other patients, the mean MK levels in drug-naive schizophrenia (0.30+/-0.10 ng/ml) were significantly (P=0.018, Fisher's protected least significant difference test) decreased than those in the controls (0.40+/-0.12 ng/ml). These suggest that there are two clusters of serum MK abnormalities in drug-naive patients with schizophrenia.