A Humoral Recognition-Behavioral Stress-Coping Glycolipid Considered As another Biomarker of Psychotic Symptoms of Schizophrenia

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引用次数: 3

Abstract

Background: Mammalians have the recognition-behavioral stress-coping system regulated via the neuronal modules followed by some humoral glycolipids. A sulfated Galbeta1-4GlcNAc-lipid which promotes the serotonergic module, keeps physical strength by regulating emotional behaviors. GalNAcalpha1-3GalNAc-lipid which promotes the adrenergic module, induces stress-coping behaviors. A sulfated Fucalpha1-2Gal-lipid protects the cholinergic module maintaining stress-coping memories from the ischemic stress. Sialalpha2-3Gal-lipid which promotes the dopaminergic module, integrates these recognition-behaviors. It is considered stresses are closely related to onset of schizophrenia, and the psychotic symptoms are not necessarily deleted after long-time medication. Schizophrenic patients might abnormally produce the humoral recognition-behavioral stress-coping glycolipids even under medication. Materials and Methods: I examined the humoral stress-coping glycolipids of medicated schizophrenic patients and those of medicated manic patients without psychotic symptoms for comparison. Results: The medicated manic patients increased sulfated Galbeta1-4GlcNAc-lipid production. The medicated schizophrenic patients increased sulfated Galbeta1-4GlcNAc-lipid production, and remarkably produced Sialalpha2- 3Gal-lipid. These indicate the manic patients and the schizophrenic patients had a stress to be coped with the serotonergic module activity, and psychotic symptoms of the schizophrenic patients would be induced via stress-coping Sialalpha2-3Gal-lipid production. Conclusion: The stressors are not clear, however, I understood humoral Sialalpha2-3Gal-lipid would be considered as another biomarker of psychotic symptoms of schizophrenia.
一种体液识别-行为应激应对糖脂被认为是精神分裂症精神病症状的另一生物标志物
背景:哺乳动物具有识别-行为应激应对系统,该系统由神经元模块和一些体液糖脂调节。一种硫酸酸化的galbeta1 - 4glcnac脂质,它能促进血清素能模块,通过调节情绪行为来保持体力。galnaalpha1 - 3galnac脂质促进肾上腺素能模块,诱导应激应对行为。硫酸化的fucalpha1 - 2gal脂质保护胆碱能模块维持缺血应激的应激应对记忆。sialalpha2 - 3gal脂质促进多巴胺能模块,整合这些识别行为。应激与精神分裂症的发病密切相关,长期服药后精神病症状不一定消失。精神分裂症患者即使在药物治疗下也可能异常地产生体液识别-行为应激应对糖脂。材料与方法:我检测了精神分裂症药物治疗患者和无精神病症状的躁狂药物治疗患者的体液应激应对糖脂,以进行比较。结果:经药物治疗的躁狂患者硫酸化galbeta1 - 4glcnac -脂质生成增加。服用药物的精神分裂症患者硫酸化galbeta1 - 4glcnac -脂质产生增加,显著地产生sialalpha2 - 3gal -脂质。这些结果表明,躁狂患者和精神分裂症患者都有应激反应需要应对这些血清素模块的活性,而精神分裂症患者的精神病症状可能是通过应激反应中sialalpha2 - 3gal -脂质的产生而诱发的。结论:应激源尚不清楚,但我了解体液唾液α 2- 3gal脂质可作为精神分裂症精神症状的另一生物标志物。
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