Abstract：
Schizophrenic individuals display disrupted myelination patterns, altered oligodendrocyte distribution, and abnormal oligodendrocyte morphology. Schizophrenia is linked with dysregulation of a variety of genes involved in oligodendrocyte function and myelin production. Single-nucleotide polymorphisms (SNPs) and rare mutations in myelination-related genes are observed in certain schizophrenic populations, representing potential genetic risk factors. Downregulation of myelination-related RNAs and proteins, particularly in frontal and limbic regions, is consistently associated with the disorder across multiple studies. These findings support the notion that disruptions in myelination may contribute to the cognitive and behavioral impairments experienced in schizophrenia, although further evidence of causation is needed.
摘要：
精神分裂症患者表现出髓鞘形成模式中断，少突胶质细胞分布改变，少突胶质细胞形态异常。精神分裂症与参与少突胶质细胞功能和髓磷脂产生的多种基因的失调有关。在某些精神分裂症人群中观察到髓鞘形成相关基因的单核苷酸多态性（SNP）和罕见突变，代表潜在的遗传风险因素。髓鞘形成相关RNA和蛋白质的下调，特别是在额叶和边缘区域，在多项研究中始终与该疾病相关。这些发现支持以下观点：髓鞘形成的中断可能会导致精神分裂症患者的认知和行为障碍。尽管还需要进一步的因果关系证据。
