作者: Francis E Lotrich , Salwa Albusaysi , Robert E Ferrell
DOI: 10.1038/NPP.2012.263
关键词:
摘要: Depression has been associated with inflammation, and inflammation may both influence interact growth factors such as brain-derived neurotrophic factor (BDNF). Both the functional Val66Met BDNF polymorphism (rs6265) levels have depression. It is thus plausible that decreased could mediate and/or moderate cytokine-induced We therefore prospectively employed Beck Inventory-II (BDI-II), Hospital Anxiety Scale (HADS), Montgomery–Asberg Rating (MADRS) in 124 initially euthymic patients during treatment interferon-alpha (IFN-α), assessing serum rs6265. Using mixed-effect repeated measures, lower pretreatment was higher depression symptoms IFN-α (F144,17.2=6.8; P<0.0001). However, although Met allele (F1,83.0=5.0; P=0.03), it only increased MADRS scores (F4,8.9=20.3; P<0.001), not BDI-II or HADS. An exploratory comparison of individual items indicated suicidal ideation, sadness, worthlessness, but neurovegetative symptoms. Conversely, serotonin transporter promoter (5-HTTLPR) short insomnia, poor appetite fatigue, ideation. therapy further lowered (F4,37.7=5.0; P=0.003), this decrease occurred regardless development. The findings do support hypothesis decreasing primary pathway by which worsens Nonetheless, results resiliency against developing inflammatory cytokine-associated depression, specifically to a subset distinct from those influenced 5-HTTLPR.