Discipline of Psychiatry, University of Adelaide, Adelaide, SA, Australia; Northern Adelaide Local Health Network, Adelaide, SA, Australia; Ramsay Health Care (SA) Mental Health, Australia.
Nutrigenomics & DNA Damage Diagnostics, CSIRO Health and Biosecurity, Adelaide, SA, Australia.
Schizophr Res. 2017 Dec;190:46-51. doi: 10.1016/j.schres.2017.03.007. Epub 2017 Mar 9.
Schizophrenia is a complex mental illness affecting the normal functioning of the brain, interfering with the ability to think, feel and act. It can be conceptualised as a syndrome of accelerated ageing, with early onset of cardiovascular disease and high rates of premature mortality. Telomere attrition increases with oxidative stress and is considered a biomarker of ageing. Previous studies have assessed abnormalities in telomere length in schizophrenia, but the results are inconsistent. The present study used a case-control design to assess whether people with schizophrenia have shortened telomeres, indicative of accelerated ageing. Subjects were all male, aged 25-35years, living in the same urban region of Adelaide, South Australia. Telomere length was measured using a quantitative real-time polymerase chain reaction (PCR) method. We found significantly shorter telomeres in people with schizophrenia relative to healthy controls. This is the first study to show telomere attrition among people with schizophrenia in Australia. Shorter telomere length may indicate the common pathways that schizophrenia shares with other neuropsychiatric and neurodevelopmental disorders associated with increased cellular senescence. Further well-controlled larger studies in people with schizophrenia are required to fully understand (i) the role of variables that have the potential to modulate telomere length such as use of antipsychotic drugs, medical conditions, parental age, smoking, alcohol abuse and use of illicit drugs; (ii) effective treatments to slow telomere erosion and (iii) mechanisms responsible for accelerating and reducing telomere damage.
精神分裂症是一种影响大脑正常功能的复杂精神疾病,干扰思维、感觉和行为能力。它可以被概念化为加速衰老的综合征,心血管疾病发病早,死亡率高。端粒损耗随着氧化应激而增加,被认为是衰老的生物标志物。先前的研究已经评估了精神分裂症中端粒长度的异常,但结果不一致。本研究采用病例对照设计,评估精神分裂症患者是否存在端粒缩短,表明加速衰老。研究对象均为男性,年龄在 25-35 岁之间,居住在南澳大利亚阿德莱德的同一城市地区。使用实时定量聚合酶链反应 (PCR) 方法测量端粒长度。我们发现精神分裂症患者的端粒明显短于健康对照组。这是第一项表明澳大利亚精神分裂症患者端粒损耗的研究。端粒缩短可能表明精神分裂症与其他神经精神和神经发育障碍共享导致细胞衰老增加的常见途径。需要在精神分裂症患者中进行更多的、精心控制的大型研究,以充分了解(i)有可能调节端粒长度的变量的作用,如使用抗精神病药物、医疗状况、父母年龄、吸烟、酗酒和使用非法药物;(ii)减缓端粒侵蚀的有效治疗方法;以及(iii)导致加速和减少端粒损伤的机制。