ABSTRACT
Objective To investigate the effects of quetiapine on serum levels of brain-derived neurotrophic factors ( BDNF) and the correlation between BDNF and psychiatric symptoms and cognitive function in patients with first-episode schizophrenia. Methods Eighty patients with first-episode schizophrenia ( treatment group) were treated with quetiapine orally for 4 weeks,at initial dose of 100 mg·d-1 and average dose of (580±120) mg·d-1 . The psychiatric symptoms were evaluated by using the positive and negative syndrome scale ( PANSS) . The cognitive function was assessed by using Wisconsin cards sort test ( WCST) . The serum BDNF level was detected with enzyme-linked immunosorbent assay ( ELISA) . Results The serum level of BDNF was markedly lower in schizophrenic patients before[(13. 72±8. 79) ng·mL-1,P<0. 01] and after treatment[(18. 02±9.06) ng·mL-1,P<0.05]in comparison with normal controls(23. 67±10. 13) ng·mL-1]. After treatment,the PANSS total scores and subscale scores decreased,WCST number of categories and the number of correct answers increased,and the number of wrong answers reduced. There was a positive correlation between the serum BDNF and negative symptoms ( SANS) ( r= 0. 54, P=0. 032),and the number of correct answers. Conclusion The quetiapine significantly increases serum level of BDNF in schizophrenia patients,which correlates positively with improvements in symptoms and cognitive function.
ABSTRACT
<p><b>OBJECTIVE</b>To assess the association of BDNF gene Val66Met polymorphism with efficacy of antidepressant treatment and plasma BDNF level.</p><p><b>METHODS</b>Two hundred and forty-nine ethnic Han Chinese patients with depression(study group), who have met the diagnostic criteria of DSM-IV, were prescribed with venlafaxine or paroxetine. Two hundred and two healthy individuals were recruited as the control group. General demographic information such as gender, age, educational status, occupation, and marriage status were collected. HAMD-17 was adopted as the primary rating tool to evaluate the severity of depression on the baseline and at the end of 1st, 2nd, 4th, 6th week of treatment. PCR-restriction fragment length polymorphism was applied to determine the Val66Met polymorphism of the BDNF gene in the two groups. Plasma BDNF concentration was measured with ELISA before and after 6 weeks of treatment.</p><p><b>RESULTS</b>No significant differences have been found in HAMD scores and reduction of HAMD scores on the baseline and at the end of 1 st, 2nd, 4th, 6th weeks of treatment for each genotype. Nor were significant differences found in the Val66Met genotypes and allelic frequency between patients who achieved remission or not after 6 weeks' treatment as well as the healthy volunteers. The plasma BDNF level in depression patients was lower than that in healthy controls. The BDNF level has increased significantly after 6 weeks' treatment with both venlafaxine and paroxetine, but was still lower than the healthy controls. The BDNF level in the patients achieved remission who were treated with venlafaxine was similar to the normal controls, while those treated with paroxetine was still lower than normal controls. The BDNF level in patients who have not achieved remission was lower than normal controls. The BDNF level was not associated with the Val66Met polymorphism on the baseline and the end of 6th week.</p><p><b>CONCLUSION</b>No association has been found between the efficacy of venlafaxine or paroxetine and the BDNF Val66Met polymorphism. The BDNF level of patients with depression is significantly lower than healthy controls on the baseline, and can be enhanced with the treatment. Particularly, the BDNF level in patients who achieved remission after the treatment of venlafaxine can rise to normal. The level of BDNF has certain value in the forecasting of efficacy in the anti-depression therapy. BDNF level is not associated with the Val66Met polymorphism of the BDNF gene.</p>