自闭症中小胶质细胞激活的证据及其在大脑连接不足中的可能作用。

Neuron glia biology Pub Date : 2011-05-01 Epub Date: 2012-07-06 DOI:10.1017/S1740925X12000142
Juan I Rodriguez, Janet K Kern
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引用次数: 159

摘要

有证据表明,患有自闭症谱系障碍(ASD)的儿童在大脑的不同区域遭受持续的神经炎症过程,涉及小胶质细胞激活。当小胶质细胞长时间保持激活状态时,介质的产生比正常情况下持续的时间更长,介质的增加导致突触连接的丧失和神经元细胞的死亡。小胶质细胞的激活会导致连接缺失或连接不足。在自闭症的许多研究中都报道了连接不足。控制神经炎症的一种方法是减少或抑制小胶质细胞的激活。通过减少脑炎症和小胶质细胞的激活,慢性炎症的神经破坏性作用可能会减少,并允许改善发育结果。未来的研究可能会减少小胶质细胞的激活和神经炎症,并最终帮助减轻ASD的症状。
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Evidence of microglial activation in autism and its possible role in brain underconnectivity.

Evidence indicates that children with autism spectrum disorder (ASD) suffer from an ongoing neuroinflammatory process in different regions of the brain involving microglial activation. When microglia remain activated for an extended period, the production of mediators is sustained longer than usual and this increase in mediators contributes to loss of synaptic connections and neuronal cell death. Microglial activation can then result in a loss of connections or underconnectivity. Underconnectivity is reported in many studies in autism. One way to control neuroinflammation is to reduce or inhibit microglial activation. It is plausible that by reducing brain inflammation and microglial activation, the neurodestructive effects of chronic inflammation could be reduced and allow for improved developmental outcomes. Future studies that examine treatments that may reduce microglial activation and neuroinflammation, and ultimately help to mitigate symptoms in ASD, are warranted.

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Neuron glia biology
Neuron glia biology 医学-神经科学
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