Metabolic counterparts of sodium accumulation in multiple sclerosis

• Verfasst von: Donadieu, Maxime [VerfasserIn]
• Verfasst von: Schad, Lothar R. [VerfasserIn]
• Titel: Metabolic counterparts of sodium accumulation in multiple sclerosis
• Titelzusatz: a whole brain 23Na-MRI and fast 1H-MRSI study
• Verf.angabe: Maxime Donadieu, Yann Le Fur, Adil Maarouf, Soraya Gherib, Ben Ridley, Lauriane Pini, Stanislas Rapacchi, Sylviane Confort-Gouny, Maxime Guye, Lothar R Schad, Andrew A Maudsley, Jean Pelletier, Bertrand Audoin, Wafaa Zaaraoui and Jean-Philippe Ranjeva
• Jahr: 2019
• Jahr des Originals: 2017
• Umfang: 19 S.
• Fussnoten: First Published October 24, 2017 ; Gesehen am 19.06.2019 ; Im Titelzusatz ist "23" und "1" hochgestellt
• Titel Quelle: Enthalten in: Multiple sclerosis journal
• Ort Quelle: London : Sage, 1995
• Jahr Quelle: 2019
• Band/Heft Quelle: 25(2019), 1, Seite 39-47
• ISSN Quelle: 1477-0970
• DOI: doi:10.1177/1352458517736146
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1577948831

Abstract

Background: Increase of brain total sodium concentrations (TSC) is present in multiple sclerosis (MS), but its pathological involvement has not been assessed yet. Objective: To determine in vivo the metabolic counterpart of brain sodium accumulation. Materials/methods: Whole brain 23Na-MR imaging and 3D-1H-EPSI data were collected in 21 relapsing-remitting multiple sclerosis (RRMS) patients and 20 volunteers. Metabolites and sodium levels were extracted from several regions of grey matter (GM), normal-appearing white matter (NAWM) and white matter (WM) T2 lesions. Metabolic and ionic levels expressed as Z-scores have been averaged over the different compartments and used to explain sodium accumulations through stepwise regression models. Results: MS patients showed significant 23Na accumulations with lower choline and glutamate-glutamine (Glx) levels in GM; 23Na accumulations with lower N-acetyl aspartate (NAA), Glx levels and higher Myo-Inositol (m-Ins) in NAWM; and higher 23Na, m-Ins levels with lower NAA in WM T2 lesions. Regression models showed associations of TSC increase with reduced NAA in GM, NAWM and T2 lesions, as well as higher total-creatine, and smaller decrease of m-Ins in T2 lesions. GM Glx levels were associated with clinical scores. Conclusion: Increase of TSC in RRMS is mainly related to neuronal mitochondrial dysfunction while dysfunction of neuro-glial interactions within GM is linked to clinical scores.