通过建模成像测量评估体内神经元代谢。
Assessing neuronal metabolism in vivo by modeling imaging measures.
机构信息
Department of Brain Repair and Rehabilitation, NMR Unit, UCL Institute of Neurology, London WC1N 3BG, United Kingdom.
出版信息
J Neurosci. 2010 Nov 10;30(45):15030-3. doi: 10.1523/JNEUROSCI.3330-10.2010.
Abstract
Mitochondrial dysfunction contributes to the pathogenesis of many neurological diseases, including multiple sclerosis (MS), but is not directly measurable in vivo. We modeled N-acetyl-aspartate (NAA), which reflects axonal structural integrity and mitochondrial metabolism, with imaging measures of axonal structural integrity (axial diffusivity and cord cross-sectional area) to extract its mitochondrial metabolic contribution. Lower residual variance in NAA, reflecting reduced mitochondrial metabolism, was associated with greater clinical disability in MS, independent of structural damage.
摘要
线粒体功能障碍是许多神经疾病（包括多发性硬化症）发病机制的原因，但在体内无法直接测量。我们用反映轴突结构完整性和线粒体代谢的 N-乙酰天门冬氨酸（NAA）建立模型，用轴突结构完整性的影像学测量（轴向扩散和脊髓横截面积）来提取其线粒体代谢的贡献。NAA 的残余方差降低，反映线粒体代谢减少，与多发性硬化症的更大临床残疾相关，与结构损伤无关。
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本文引用的文献
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