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In (deficit) schizophrenia, a general cognitive decline (G-CoDe) partly mediates the effects of neuro-immune and neuro-oxidative toxicity on the symptomatome and quality of life.
medRxiv - Psychiatry and Clinical Psychology Pub Date : 2021-04-06 , DOI: 10.1101/2021.03.29.21254523
Michael Maes , Buranee Kanchanatawan

Objective: Schizophrenia and deficit schizophrenia are accompanied by neurocognitive impairments. The aim of this study was to examine whether a general factor underpins impairments in key Cambridge Neuropsychological Test Automated Battery (CANTAB) probes, verbal fluency (VFT), world list memory (WLM), true recall, and Mini Mental State Examination (MMSE). Methods: We recruited 80 patients with schizophrenia and 40 healthy controls. All patients were assessed using CANTAB tests, namely paired-association learning (PAL), rapid visual information (RVP), spatial working memory (SWM), one touch stocking (OTS), intra/extradimensional set shifting (IED), and emotional recognition test (ERT). Results: We found that a general factor, which is essentially unidimensional, underlies those CANTAB, VFT, WLM, True Recall, and MMSE scores. This common factor shows excellent psychometric properties and fits a reflective model and, therefore, reflects a general cognitive decline (G-CoDe) comprising deficits in semantic and episodic memory, recall, executive functions, strategy use, rule acquisition, visual sustained attention, attention set-shifting, and emotional recognition. Partial least Square analysis showed that 40.5% of the variance in G-Code is explained by CCL11, IgA to tryptophan catabolites, and increased oxidative toxicity; and that G-CoDe explains 44.8% of the variance in a general factor extracted from psychosis, hostility, excitation, mannerism, negative symptoms, formal thought disorders, and psychomotor retardation; and 40.9% in quality of life scores. The G-CoDe is significantly greater in deficit than in nondeficit schizophrenia. Conclusions: A common core shared by a multitude of neurocognitive impairments (G-CoDe) mediates the effects of neurotoxic pathways on the phenome of (deficit) schizophrenia.

中文翻译:

在(精神分裂症)精神分裂症中,一般性认知能力下降(G-CoDe)部分介导了神经免疫和神经氧化毒性对症状组和生活质量的影响。

目的:精神分裂症和精神分裂症伴有神经认知障碍。这项研究的目的是检查通用因素是否支持关键的剑桥神经心理测试自动电池(CANTAB)探针,口语流利性(VFT),世界列表记忆(WLM),真实回忆和迷你精神状态检查(MMSE) 。方法:我们招募了80位精神分裂症患者和40位健康对照。所有患者均使用CANTAB测试进行评估,即配对联想学习(PAL),快速视觉信息(RVP),空间工作记忆(SWM),一键储存(OTS),内/外维度移位(IED)和情绪识别测试(ERT)。结果:我们发现,一个基本因素基本上是一维的,它是那些CANTAB,VFT,WLM,True Recall和MMSE得分的基础。这个共同因素显示出优异的心理测量特性并符合反射模型,因此反映了一般性认知下降(G-CoDe),包括语义和情景记忆,回忆,执行功能,策略使用,规则获取,视觉持续注意力,注意力的缺陷设定转变和情感认同。偏最小二乘分析表明,CCL11,IgA对色氨酸分解代谢产物和氧化毒性的增加解释了G码中40.5%的变异。并且G-CoDe解释了从精神病,敌对,兴奋,举止,消极症状,正式思想障碍和精神运动发育迟缓中提取的一般因素中44.8%的方差;生活质量得分为40.9%。与非赤字型精神分裂症相比,G-CoDe的赤字明显更大。结论:
更新日期:2021-04-08
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