Brunelin Jerome, d'Amato Thierry, van Os Jim, Cochet Alain, Suaud-Chagny Marie-Françoise, Saoud Mohamed
Université de Lyon, Lyon, F-69003, France; Université Lyon 1, Lyon, EA4166; CH Le Vinatier, Bron, F-69677, France.
Schizophr Res. 2008 Mar;100(1-3):206-11. doi: 10.1016/j.schres.2007.11.009. Epub 2007 Dec 21.
A genetically mediated abnormal sensitivity to stress is thought to play a role in the onset, exacerbation and relapse of schizophrenia. In a double blind, placebo-controlled crossover study, peak increases in plasma ACTH (Delta ACTH) and homovanillic-acid, a dopamine metabolite, (Delta HVA) following exposure to a metabolic stressor(2DG) were studied in unaffected siblings of patients with schizophrenia (n=15), their patient relatives (n=15) and healthy controls (n=14). Siblings showed a stress response (both Delta ACTH and Delta HVA) that was significantly greater compared to controls and significantly less pronounced compared to patients. The results suggest that the genetic risk for schizophrenia may be characterized by an enhanced sensitivity to stress.
基因介导的对应激异常敏感被认为在精神分裂症的起病、加重及复发中起作用。在一项双盲、安慰剂对照的交叉研究中，研究了精神分裂症患者的未患病同胞（n = 15）、患者亲属（n = 15）及健康对照（n = 14）在暴露于代谢应激源（2-脱氧葡萄糖）后血浆促肾上腺皮质激素峰值升高（Δ促肾上腺皮质激素）及多巴胺代谢产物高香草酸（Δ高香草酸）的情况。同胞表现出的应激反应（Δ促肾上腺皮质激素和Δ高香草酸）与对照相比显著增强，与患者相比则显著减弱。结果表明，精神分裂症的遗传风险可能表现为对应激的敏感性增强。
