The therapeutic effect of ginkgo biloba extract for male patients with tardive dyskinesia: the role of brain-derived neurotrophic factor genotypes / 中华行为医学与脑科学杂志

ABSTRACT

Objective:To investigate whether ginkgo biloba extract(EGb) can improve the symptoms of tardive dyskinesia(TD) by increasing the levels of serum brain-derived neurotrophic factor (BDNF), and to explore whether the BDNF Val66Met genotype can influence the efficacy of TD by EGb.Methods:A total of 78 male schizophrenia inpatients with TD were enrolled, and 77 patients completed 12 weeks of treatment with EGb(240 mg/d). The abnormal involuntary movement scale (AIMS), positive and negative syndrome scale (PANSS) and serum BDNF levels were measured at before and after 12 weeks of treatment.Serum BDNF levels were measured by enzyme linked immunosorbent assay (Elisa). In addition, the BDNF Val66Met polymorphism was genotyped by the method of PCR-restriction fragment length polymorphism (PCR-RFLP) in all patients.Results:Compared with before treatment, the scores of total AIMS((7.0±2.9) vs (4.9±2.2)), total PANSS ((55.8±14.0) vs(51.1±9.7)), subscale P((9.6±3.3) vs (8.6±2.2)), subscale N((23.2±8.3) vs (21.4±6.3)) and subscale G((23.0±4.9) vs (21.1±2.7)) were significantly decreased( P<0.01), while the levels of BDNF were significantly increased((10.8±2.9)μg/L vs (9.6±3.3)μg/L, P<0.05) in TD patients after treatment.The increased level of BDNF was positively correlated with the decrease of AIMS( r=0.28, P=0.014), but no significantly correlated with the improvement of PANSS total scores and the three subscales were found(all P>0.05). After treatment, the decrease of AIMS in patients with Val/Val genotype was significantly greater than that in patients with Val allele (Met/Val plus Met/Met genotype) (both P<0.05). Further analysis showed that only patients with Val/Met heterozygotes had a significant increase in BDNF levels after treatment ( P<0.05). Conclusions:EGb may improve TD symptoms through neuroprotective and regulatory effects.The BDNF genotype is involved in regulating the efficacy of EGb in the treatment of TD, which may be related to its regulation of BDNF serum levels.