Varhaug Kristin N, Vedeler Christian A, Myhr Kjell-Morten, Aarseth Jan Harald, Tzoulis Charalampos, Bindoff Laurence A
Department of Neurology, Haukeland University Hospital, Bergen, Norway; KG Jebsen Centre of MS Research, Department of Clinical Medicine, University of Bergen, Bergen, Norway; Department of Clinical Medicine (K1), University of Bergen, Bergen, Norway.
Department of Neurology, Haukeland University Hospital, Bergen, Norway; KG Jebsen Centre of MS Research, Department of Clinical Medicine, University of Bergen, Bergen, Norway; Norwegian MS-Registry & Biobank, Department of Neurology, Haukeland University Hospital, Bergen, Norway; Department of Clinical Medicine (K1), University of Bergen, Bergen, Norway.
Mitochondrion. 2017 May;34:32-35. doi: 10.1016/j.mito.2016.12.003. Epub 2016 Dec 23.
Mitochondrial DNA (mtDNA) can act as damage-associated molecular pattern molecule (DAMP) and initiate an inflammatory response. We hypothesized that the concentration of mtDNA might reflect inflammatory activity in multiple sclerosis and investigated therefore levels of cell-free mitochondrial DNA in cerebrospinal fluid of patients with relapsing-remitting multiple sclerosis. Significantly higher levels of mtDNA were found in patients compared to controls and there was an inverse correlation between disease duration and mtDNA concentration. Our study suggests that mitochondria can be involved early in multiple sclerosis, but whether this is as an initiator of the inflammatory response or part of its maintenance is unclear. Further, our study suggests that changes in mtDNA may provide a novel marker for early disease activity.
线粒体DNA(mtDNA)可作为损伤相关分子模式分子(DAMP)并引发炎症反应。我们推测mtDNA的浓度可能反映多发性硬化症中的炎症活动,因此研究了复发缓解型多发性硬化症患者脑脊液中游离线粒体DNA的水平。与对照组相比,患者体内mtDNA水平显著更高,且病程与mtDNA浓度呈负相关。我们的研究表明,线粒体可能在多发性硬化症早期就参与其中,但这是作为炎症反应的启动因素还是其维持的一部分尚不清楚。此外,我们的研究表明,mtDNA的变化可能为疾病早期活动提供一个新的标志物。