Conte Center for the Neuroscience of Mental Disorders and the Department of Psychiatry, Mount Sinai School of Medicine, New York, NY 10029, USA.
Prog Neurobiol. 2011 Jan;93(1):13-24. doi: 10.1016/j.pneurobio.2010.09.004. Epub 2010 Oct 13.
Multiple lines of evidence in schizophrenia, from brain imaging, studies in postmortem brains, and genetic association studies, have implicated oligodendrocyte and myelin dysfunction in this disease. Recent studies suggest that oligodendrocyte and myelin dysfunction leads to changes in synaptic formation and function, which could lead to cognitive dysfunction, a core symptom of schizophrenia. Furthermore, there is accumulating data linking oligodendrocyte and myelin dysfunction with dopamine and glutamate abnormalities, both of which are found in schizophrenia. These findings implicate oligodendrocyte and myelin dysfunction as a primary change in schizophrenia, not only as secondary consequences of the illness or treatment. Strategies targeting oligodendrocyte and myelin abnormalities could therefore provide therapeutic opportunities for patients suffering from schizophrenia.
多项证据表明，精神分裂症与少突胶质细胞和髓鞘功能障碍有关，这些证据来自脑影像学、尸检大脑研究和遗传关联研究。最近的研究表明，少突胶质细胞和髓鞘功能障碍导致突触形成和功能发生变化，从而导致认知功能障碍，这是精神分裂症的核心症状。此外，越来越多的数据表明，少突胶质细胞和髓鞘功能障碍与多巴胺和谷氨酸异常有关，这两种异常在精神分裂症中都存在。这些发现表明，少突胶质细胞和髓鞘功能障碍是精神分裂症的主要变化，不仅是疾病或治疗的次要后果。因此，针对少突胶质细胞和髓鞘异常的策略可能为精神分裂症患者提供治疗机会。
