Association of the C(-1019)G 5-HT1A functional promoter polymorphism with antidepressant response.

摘要: Antidepressants, such as serotonin or noradrenaline reuptake inhibitors (e.g. fluoxetine, nefadozone) 5-HT1A agonists (flibanserin), desensitize the autoreceptor, which may contribute to their clinical efficacy. The receptor gene is repressed by NUDR/DEAF-1 in raphe cells at C-, but not G-allele of C(-1019)G polymorphism that associated with major depression and suicide. Depressed patients (n=118) were treated antidepressants including fluoxetine nefadozone combined pindolol flibanserin alone. severity was assesssed using Hamilton Rating Scale for Depression. Although had similar initially, those homozygous G(-1019) genotype responded significantly less (p=0.039) pooled antidepressant treatment groups (p=0.0497) approximately twice likely be non-responders C(-1019)C genotype. These results implicate a potential marker response, suggesting role repression gene.