多发性硬化症中脑氧消耗与年龄相关的下降
Maria H Knudsen1,2, Mark B Vestergaard1, Ulrich Lindberg1
1Functional Imaging Unit, Dept. of Clinical Physiology and Nuclear Medicine, Copenhagen University Hospital - Rigshospitalet, Glostrup, Denmark.
概括
在早期复发性缓解性多发性硬化症 (RRMS) 中,大脑的氧化代谢减少,这是由细胞呼吸问题驱动的,而不是缩或血液流量减少. 这一发现凸显了RRMS的潜在新治疗点.
科学领域:
- 神经科学是一个神经科学.
- 医疗成像医学成像
- 代谢研究研究 代谢研究
背景情况:
- 在复发性缓解性多发性硬化症 (RRMS) 中,大脑的氧气代谢发生变化.
- 可能的原因包括与疾病相关的脑缩或MS诱导的炎症抑制大脑代谢.
研究的目的:
- 在早期RRMS患者中测量大脑血流 (CBF) 和大脑氧气代谢率 (CMRO2).
- 研究CMRO2,脑缩,病变负载和RRMS中残疾之间的关系.
主要方法:
- 利用MRI相位对比映射和基于敏感性的氧度测量来测量CBF和CMRO2.
- 评估大脑缩和白质病变负载使用高分辨率结构MRI.
- 从患者记录中收集扩展残疾状况量表 (EDSS) 的得分.
主要成果:
- 与对照组相比,RRMS患者的CMRO2显著降低 (-15%).
- 在RRMS患者中,CMRO2随着年龄的增长而下降.
- 较低的CMRO2与更高的静脉氧和有关,而不是降低CBF.
- 没有发现大脑缩或CMRO2与病变负载/EDSS之间的相关性有显著差异.
结论:
- 在早期RRMS中,渐进的CMRO2下降独立于显著的大脑缩和充足的CBF.
- 功能障碍的细胞呼吸是RRMS中潜在的致病机制和治疗点.
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