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Lancet neurol:神经炎症在快速动眼睡眠障碍中发挥什么样的作用

2017-07-04 qinqiyun MedSci原创

对快速动眼睡眠障碍患者(IRBD)的长期随访研究发现多数患者最终会进展成共核蛋白帕金森病、痴呆或者多系统萎缩。在共核蛋白中发现小胶质神经细胞活动的神经炎症,考虑其或许可以成为终止或延迟神经退行性变进程的潜在治疗靶点。

背景:对快速动眼睡眠障碍患者(IRBD)的长期随访研究发现多数患者最终会进展成共核蛋白帕金森病、痴呆或者多系统萎缩。在共核蛋白中发现小胶质神经细胞活动的神经炎症,考虑其或许可以成为终止或延迟神经退行性变进程的潜在治疗靶点。研究者们致力于探究IRBD患者是否有神经炎症以及神经炎症与黑质多巴胺功能的关系。

方法:2015年3月23日-2016年10月19日,招募20位尚未有临床确诊的帕金森病和认知障碍的IRBD患者和19位没有运动和认知障碍、神经学检查正常、平均年龄与IRBD患者组相当的健康对照。对于IRBD患者, 用11C-PK11195 PET检查小胶质神经细胞在黑质、壳核和尾状核的活性,并用18F-DOPA PET检查壳核和尾状核的多巴胺轴末端功能。对照组接受11C-PK11195 PET检查或18F-DOPA PET检查。然后比较两组18F-DOPA的摄取量和11C-PK11195结合潜能。

结果:与对照组相比,IRBD患者左侧的黑质区域的11C-PK11195结合率增加,而在右侧黑质、壳核和尾状核则没有明显改变。IRBD患者的两侧壳核的18F-DOPA摄取率均增加,在尾状核则没有改变。

分析:IRBD患者,黑质区域小胶质神经细胞活性增加伴随壳核多巴胺功能下降。需要包含更多样本量的长期深入研究来验证本文的成果,并评估IRBD患者体内的活动性小胶质神经细胞的出现是否可以作为短期内会发展成蛋白质病的标志物。

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    2018-03-11 howi
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    2017-07-05 yinhl1978

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