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首页> 外文期刊>Biological psychiatry >Microglial activation and increased microglial density observed in the dorsolateral prefrontal cortex in autism.
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Microglial activation and increased microglial density observed in the dorsolateral prefrontal cortex in autism.

机译：在自闭症的背外侧前额叶皮层中观察到小胶质细胞活化和小胶质细胞密度增加。

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BACKGROUND: In the neurodevelopmental disorder autism, several neuroimmune abnormalities have been reported. However, it is unknown whether microglial somal volume or density are altered in the cortex and whether any alteration is associated with age or other potential covariates. METHODS: Microglia in sections from the dorsolateral prefrontal cortex of nonmacrencephalic male cases with autism (n = 13) and control cases (n = 9) were visualized via ionized calcium binding adapter molecule 1 immunohistochemistry. In addition to a neuropathological assessment, microglial cell density was stereologically estimated via optical fractionator and average somal volume was quantified via isotropic nucleator. RESULTS: Microglia appeared markedly activated in 5 of 13 cases with autism, including 2 of 3 under age 6, and marginally activated in an additional 4 of 13 cases. Morphological alterations included somal enlargement, process retraction and thickening, and extension of filopodia from processes. Average microglial somal volume was significantly increased in white matter (p = .013), with a trend in gray matter (p = .098). Microglial cell density was increased in gray matter (p = .002). Seizure history did not influence any activation measure. CONCLUSIONS: The activation profile described represents a neuropathological alteration in a sizeable fraction of cases with autism. Given its early presence, microglial activation may play a central role in the pathogenesis of autism in a substantial proportion of patients. Alternatively, activation may represent a response of the innate neuroimmune system to synaptic, neuronal, or neuronal network disturbances, or reflect genetic and/or environmental abnormalities impacting multiple cellular populations.
机译：背景：在神经发育障碍自闭症中，已报道了几种神经免疫异常。但是，尚不清楚皮层中小胶质细胞的体积或密度是否改变，以及年龄或其他潜在的协变量是否与任何改变有关。方法：通过电离钙结合衔接子分子1免疫组织化学观察非自发性自发性非脑性男性病例的背外侧前额叶皮层中的小胶质细胞（n = 13）和对照组（n = 9）。除神经病理学评估外，还通过光学分级仪对小胶质细胞密度进行了立体评估，并通过各向同性成核器对平均体细胞体积进行了定量。结果：小胶质细胞似乎在13例自闭症患者中有明显激活，包括6岁以下3例中的2例，在13例中另外4例中略有激活。形态学改变包括体细胞增大，过程回缩和增厚以及从过程中延伸出丝状伪足。白质中的平均小胶质体体积显着增加（p = .013），而灰质中有趋势（p = .098）。灰质中小胶质细胞密度增加（p = .002）。癫痫发作史不影响任何激活措施。结论：所描述的激活模式代表了自闭症病例中相当一部分的神经病理学改变。考虑到它的早期存在，小胶质细胞激活可能在很大比例的患者中在自闭症的发病机理中起重要作用。或者，激活可以代表先天神经免疫系统对突触，神经元或神经元网络障碍的反应，或反映影响多个细胞群体的遗传和/或环境异常。

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