Mukaetova-Ladinska E B, Arnold H, Jaros E, Perry R, Perry E
Research Neuropathology Laboratory, University of Newcastle, Newcastle Upon Tyne, UK.
Neuropathol Appl Neurobiol. 2004 Dec;30(6):615-23. doi: 10.1111/j.1365-2990.2004.00574.x.
The neuropathological substrates underlying the characteristic clinical phenotype of autism are unknown. Neuroimaging studies have identified a decrease in task-related activation in the dorsolateral prefrontal cortex in autism. In the current study, we have analysed the dorsolateral prefrontal cortex in two adult individuals with a clinical diagnosis of autism, using Nissl staining and MAP2 immunohistochemistry. There was unchanged density of both neuronal and glial cell pools, although the autistic individuals had ill-defined neocortical cellular layers, substantially depleted MAP2 neuronal expression, and reduced dendrite numbers. Further studies on a larger number of individuals with autism are needed to establish the clinical relevance of the described changes, especially to determine whether the loss of dendritic markers is age associated or disease specific.
自闭症特征性临床表型背后的神经病理学基质尚不清楚。神经影像学研究已发现自闭症患者背外侧前额叶皮质与任务相关的激活减少。在本研究中,我们使用尼氏染色和微管相关蛋白2(MAP2)免疫组织化学方法,对两名临床诊断为自闭症的成年个体的背外侧前额叶皮质进行了分析。尽管自闭症个体的新皮质细胞层界限不清、MAP2神经元表达大量减少且树突数量减少,但神经元和神经胶质细胞池的密度并未改变。需要对更多自闭症个体进行进一步研究,以确定上述变化的临床相关性,特别是要确定树突标记物的丧失是否与年龄相关或疾病特异性相关。