STUDIES OF THE IMMUNE SYSTEM IN SCHIZOPHRENIA

我们建议调查精神分裂症患者的免疫系统， 找出是否存在任何异常， 对照患者。 已经确定一些精神分裂症患者 严重迟发性运动障碍（TD）患者的抗体滴度升高， 乙酰胆碱受体的抗体 这些针对受体的抗体 因为可以纯化和标记受体; 但滴度虽然显著，但很低，这可能不一定 与TD或精神分裂症中乙酰胆碱受体有关。 这些 患者无重症肌无力的临床体征。 神经安定 药物可能会通过以下方式诱导整个自身抗体谱： 刺激免疫系统的细胞或通过作用于细胞膜， 使蛋白质成分具有抗原性。 此类抗体 很难检测，因为我们不知道它们所对应的抗原。 都是有目的的 将通过测量进一步探索这种可能性 抗体亚类、T细胞亚群、抗脑抗体和抗核抗体 抗体的 由于抗精神病药物被认为是导致TD的原因， 治疗有和没有TD的患者。 长期服用这种药物 对大鼠使用长达6个月的药物， 这与人类的TD相似。 我们将检查 这些动物中存在抗神经元抗体或淋巴细胞的证据， 可能导致神经系统变化的大脑 运动障碍

We propose to investigate the immune system in schizophrenics in order to find out if any abnormalities are present in comparison to the appropriate control patients. It has already been determined that some schizophrenic patients with severe tardive dyskinesia (TD) have elevated antibody titers against human acetylcholine receptor. These antibodies against receptor were discovered because it is possible to purify and label the receptor; but the titers, although significant, were low and this may not necessarily implicate acetylcholine receptors in TD or in schizophrenia. These patients had no clinical signs of Myasthenia Gravis. Neuroleptic medication may induce a whole spectrum of autoantibodies either by stimulating cells of the immune system or by acting upon cell membranes in such a way that protein components are rendered antigenic. Such antibodies would be difficult to detect as we do not know the antigens to which they are directed. This possibility will be further explored by measuring antibody subclasses, T-cell subsets, anti-brain antibodies and anti-nuclear antibodies. As neuroleptics are thought to cause TD we will compare drug treated patients with and without TD. The chronic administration of such drugs to rats for as long as 6 months results in an orofacial syndrome which bears resemblance to TD in humans. We will examine the brains of such animals for evidence of anti-neuronal antibodies or lymphocytes in the brain which could be responsible for the neurological changes which cause the dyskinesia.