CHMP2B 介导的额颞叶痴呆的炎症标志物。
Inflammatory markers of CHMP2B-mediated frontotemporal dementia.
机构信息
Danish Dementia Research Centre, Department of Neurology, Rigshospitalet, University of Copenhagen, Denmark.
Danish Multiple Sclerosis Center, University of Copenhagen, Department of Neurology, Rigshospitalet, Denmark.
出版信息
J Neuroimmunol. 2018 Nov 15;324:136-142. doi: 10.1016/j.jneuroim.2018.08.009. Epub 2018 Aug 17.
Histopathological studies and animal models have suggested an inflammatory component in the pathomechanism of the CHMP2B associated frontotemporal dementia (FTD-3). In this cross-sectional study, serum and cerebrospinal fluid were analyzed for inflammatory markers in CHMP2B mutation carriers. Serum levels of CCL4 were increased throughout life. Serum levels of IL-15, CXCL10, CCL22 and TNF-α were significantly associated with cognitive decline, suggesting a peripheral inflammatory response to neurodegeneration. CSF levels of sTREM2 appeared to increase more rapidly with age in CHMP2B mutation carriers. The identification of a peripheral inflammatory response to disease progression supports the involvement of an inflammatory component in FTD-3.
组织病理学研究和动物模型表明，CHMP2B 相关额颞叶痴呆（FTD-3）的发病机制中存在炎症成分。在这项横断面研究中，分析了 CHMP2B 突变携带者的血清和脑脊液中的炎症标志物。CCL4 的血清水平在整个生命周期中都增加。IL-15、CXCL10、CCL22 和 TNF-α 的血清水平与认知能力下降显著相关，提示存在针对神经退行性变的外周炎症反应。CHMP2B 突变携带者的 CSF 中 sTREM2 水平似乎随着年龄的增长而更快地增加。对疾病进展的外周炎症反应的鉴定支持 FTD-3 中存在炎症成分。
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