Abstract
We explored the effect of the Brain-derived neurotrophic factor (BDNF) Val66Met polymorphism (rs6265) on correlation between changes in plasma BDNF levels with cognitive function and quality of life (QoL) after 12 weeks of treatment in bipolar disorder (BD). Symptom severity and plasma BDNF levels were assessed upon recruitment and during weeks 1, 2, 4, 8 and 12. QoL, the Wisconsin Card Sorting Test (WCST), and the Conners’ Continuous Performance Test (CPT) were assessed at baseline and endpoint. The BDNF Val66Met polymorphism was genotyped. Changes in cognitive function and QoL over 12 weeks were reduced using factor analysis for the evaluation of their correlations with changes in plasma BDNF. Five hundred forty-one BD patients were recruited and 65.6% of them completed the 12-week follow-up. Changes in plasma BDNF levels with factor 1 (WCST) were significantly negatively correlated (r = −0.25, p = 0.00037). After stratification of BD subtypes and BDNF genotypes, this correlation was significant only in BP-I and the Val/Met genotype (r = −0.54, p = 0.008). We concluded that changes in plasma BDNF levels significantly correlated with changes in WCST scores in BD and is moderated by the BDNF Val66Met polymorphism and the subtype of BD.
Highlights
In the brain area regulating memory and emotion: the cortex and hippocampus[7]
There was a significant attenuation of clinical severity (HDRS and Young Mania Rating Scale (YMRS)) and improvement in several subscores of the Wisconsin Card Sorting Test (WCST), Continuous Performance Test (CPT), and WHOQOL after 12 weeks of treatment (Table 1)
We found a significant correlation between improvements in WCST scores and increases in plasma Brain-derived neurotrophic factor (BDNF) levels in all subtypes of Bipolar disorder (BD)
Summary
In the brain area regulating memory and emotion: the cortex and hippocampus[7]. BDNF may play an important role in the pathogenesis of BD4,8. Some researchers[30] have suggested that cognitive impairment in euthymic patients with BD might be associated with the underlying pathophysiology of BD, such as neurodegeneration and a decrease in BDNF expression levels. Most studies have focused on the cross-sectional association, not the longitudinal association of changes in cognitive function and QoL with change of plasma BDNF levels or the influence of the BDNF Val66Met polymorphism. From longitudinal design, we will be able to detect the correlation of changes in plasma BDNF and changes in cognitive function and QoL from within-individual perspective. The aims of this study were to investigate the correlation of longitudinal changes in plasma BDNF levels with longitudinal changes of cognitive function and QoL stratified by the BDNF Val66Met polymorphism in a 12-week follow-up study in patients with BD
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