Tian Li, Tan Yunlong, Chen Dachun, Lv Menghan, Tan Shuping, Soares Jair C, Zhang Xiang Yang
Neuroscience Center, Viikinkaari 4, FIN-00014, University of Helsinki, Helsinki, Finland; Beijing HuiLongGuan Hospital, Peking University, Beijing, China.
Beijing HuiLongGuan Hospital, Peking University, Beijing, China.
Prog Neuropsychopharmacol Biol Psychiatry. 2014 Oct 3;54:259-64. doi: 10.1016/j.pnpbp.2014.06.012. Epub 2014 Jul 2.
Mounting evidences have demonstrated the association of altered immune factors with neurodevelopmental and pathological progression of schizophrenia. However, whether immune factors play any role in the pathogenesis of tardive dyskinesia (TD) has been underexplored. To our best knowledge, ours is among the piloting studies examining the association of TNF alpha with extrapyramidal symptoms of schizophrenic patients so far.
The aim of this study was to assess the clinical significance of serum TNF alpha level in chronic schizophrenia, especially its potential association with TD.
Serum TNF alpha level was measured in a sandwich enzyme-linked immunosorbent assay (ELISA) from 46 medicated chronic schizophrenia patients with TD, 43 chronic schizophrenia patients without TD, and 43 healthy control subjects. The symptoms of schizophrenia were assessed by the positive and negative syndrome scale (PANSS).
Chronic patients both with TD and without TD had significantly lower serum level of TNF alpha than controls (TD=9.5±2.1pg/ml, non-TD=10.7±1.8pg/ml, control=37.8±3.4pg/ml, p<0.001). Compared to patients without TD, TD patients showed marginally significant reduction in the serum TNF alpha level (p=0.05). The reduced TNF alpha level was not significantly affected by daily dose or duration of antipsychotic drugs (p>0.05). Serum TNF alpha level was negatively correlated with the PANSS total score in the whole schizophrenia patients (p<0.01), but no significant association with TD severity was observed.
Our results suggested that at chronic stage, serum TNF activity is associated with psychopathology of schizophrenia patients, but whether it can be a biomarker for TD needs further clarification in the future.
越来越多的证据表明,免疫因子的改变与精神分裂症的神经发育及病理进展相关。然而,免疫因子在迟发性运动障碍(TD)发病机制中是否发挥作用尚未得到充分研究。据我们所知,我们的研究是目前探讨肿瘤坏死因子α(TNFα)与精神分裂症患者锥体外系症状之间关联的初步研究之一。
本研究旨在评估血清TNFα水平在慢性精神分裂症中的临床意义,尤其是其与TD的潜在关联。
采用夹心酶联免疫吸附测定法(ELISA)检测46例患有TD的药物治疗慢性精神分裂症患者、43例无TD的慢性精神分裂症患者和43例健康对照者的血清TNFα水平。采用阳性和阴性症状量表(PANSS)评估精神分裂症症状。
患有TD和未患有TD的慢性患者血清TNFα水平均显著低于对照组(TD组=9.5±2.1pg/ml,非TD组=10.7±1.8pg/ml,对照组=37.8±3.4pg/ml,p<0.001)。与无TD的患者相比,TD患者血清TNFα水平略有显著降低(p=0.05)。TNFα水平降低不受抗精神病药物每日剂量或使用时间的显著影响(p>0.05)。在整个精神分裂症患者中,血清TNFα水平与PANSS总分呈负相关(p<0.01),但未观察到与TD严重程度有显著关联。
我们的结果表明,在慢性期,血清TNF活性与精神分裂症患者的精神病理学相关,但它是否可作为TD的生物标志物,未来还需要进一步明确。