Evidence for putative pathophysiological mechanisms of autism spectrum disorder (ASD), including peripheral inflammation, blood–brain barrier disruption, white matter alterations, and abnormal synaptic overgrowth, indicate a possible involvement of neuroinflammation in the disorder. Neuroinflammation plays a role in the development and maintenance of the dendritic spines involved in glutamatergic and GABAergic neurotransmission, and also influences blood–brain permeability. Cytokines released from microglia can impact the length, location or organization of dendritic spines on excitatory and inhibitory cells as well as recruit and impact glial cell function around the neurons. In this study, gene expression levels of anti‐ and pro‐inflammatory signaling molecules, as well as oligodendrocyte and astrocyte marker proteins, were measured in both gray and white matter tissue in the anterior cingulate cortex from ASD and age‐matched typically developing (TD) control brain donors, ranging from ages 4 to 37 years. Expression levels of the pro‐inflammatory gene, HLA‐DR, were significantly reduced in gray matter and expression levels of the anti‐inflammatory gene MRC1 were significantly elevated in white matter from ASD donors as compared to TD donors, but neither retained statistical significance after correction for multiple comparisons. Modest trends toward differences in expression levels were also observed for the pro‐inflammatory (CD68, IL1β) and anti‐inflammatory genes (IGF1, IGF1R) comparing ASD donors to TD donors. The direction of gene expression changes comparing ASD to TD donors did not reveal consistent findings implicating an elevated pro‐ or anti‐inflammatory state in ASD. However, altered expression of pro‐ and anti‐inflammatory gene expression indicates some involvement of neuroinflammation in ASD. Autism Res 2020, 13: 870‐884. © 2020 The Authors. Autism Research published by International Society for Autism Research and Wiley Periodicals LLC

中文翻译：

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患有自闭症谱系障碍的男性前扣带皮层白质和灰质的神经炎症基因表达变化。


自闭症谱系障碍（ASD）的假定病理生理机制的证据，包括周围炎症、血脑屏障破坏、白质改变和异常突触过度生长，表明该疾病可能涉及神经炎症。神经炎症在参与谷氨酸能和 GABA 能神经传递的树突棘的发育和维持中发挥作用，并且还影响血脑通透性。小胶质细胞释放的细胞因子可以影响兴奋性和抑制性细胞上树突棘的长度、位置或组织，并募集和影响神经元周围的胶质细胞功能。在这项研究中，测量了 ASD 和年龄匹配的典型发育（TD）前扣带皮层灰质和白质组织中抗炎和促炎信号分子以及少突胶质细胞和星形胶质细胞标记蛋白的基因表达水平）控制大脑捐献者，年龄从 4 岁到 37 岁不等。与 TD 供体相比，ASD 供体的灰质中促炎基因HLA-DR的表达水平显着降低，而白质中抗炎基因MRC1的表达水平显着升高，但术后两者均未保持统计学显着性。多重比较的校正。比较 ASD 供体和 TD 供体，促炎基因（ CD68 、 IL1β ）和抗炎基因（ IGF1 、 IGF1R ）的表达水平也有适度的差异趋势。比较 ASD 和 TD 供体的基因表达变化方向并没有揭示出一致的发现，表明 ASD 的促炎或抗炎状态升高。 然而，促炎和抗炎基因表达的改变表明自闭症谱系障碍中神经炎症有一定参与。自闭症研究2020，13 ：870-884。 © 2020 作者。自闭症研究由国际自闭症研究协会和 Wiley periodicals LLC 出版