孤独症患者脑内神经胶质细胞的激活和神经炎症

作     者：Vargas D.L. Nascimbene C. Krishnan C. C.A. Pardo 郭俊 

作者机构：Department of N eurology Johns Hopkins Univ. Sch. of Medicine Pathology 627 600 North Wolfe S treet Baltimore MD 21287 United States Dr. 

出 版 物：《世界核心医学期刊文摘（神经病学分册）》 (Digest of the World Core Medical Journals:Clinical Neurology)

年 卷 期：2005年第1卷第5期

页      面：14-14页

学科分类：1002[医学-临床医学] 100205[医学-精神病与精神卫生学] 10[医学] 

主　　题：孤独症 神经胶质细胞 发育障碍性疾病 社会交往障碍 智力低下 细胞因子 免疫细胞化学 免疫介导 巨噬细胞 扣带回 

摘      要：Autism is a neurodevelopmental disorder characterized by impaired communicati on and social interaction and may be accompanied by mental retardation and epile psy. Its cause remains unknown, despite evidence that genetic, environmental, an d immunological factors may play a role in its pathogenesis. To investigate whet her immune mediated mechanisms are involved in the pathogenesis of autism, we used immunocytochemistry, cytokine protein arrays, and enzyme linked immunosor bent assays to study brain tissues and cerebrospinal fluid (CSF) from autistic p atients and determined the magnitude of neuroglial and inflammatory reactions an d their cytokine expression profiles. Brain tissues from cerebellum, midfrontal, and cingulate gyrus obtained at autopsy from 11 patients with autism were used for morphological studies. Fresh frozen tissues available from seven patients and CSF from six living autistic patients were used for cytokine protein profili ng. We demonstrate an active neuroinflammatory process in the cerebral cortex, w hite matter, and notably in cerebellum of autistic patients. Immunocytochemical studies showed marked activation of microglia and astroglia, and cytokine profil ing indicated that macrophage chemoattractant protein (MCP) 1 and tumor growth factor β 1, derived from neuroglia, were the most prevalent cytokines in bra in tissues. CSF showed a unique proinflammatory profile of cytokines, including a marked increase in MCP 1. Our findings indicate that innate neuroimmune reac tions play a pathogenic role in an undefined proportion of autistic patients, su ggesting that future therapies might involve modifying neuroglial responses in t he brain.