D
Don J. Mahad
Researcher at University of Edinburgh
Publications - 61
Citations - 6825
Don J. Mahad is an academic researcher from University of Edinburgh. The author has contributed to research in topics: Multiple sclerosis & Mitochondrion. The author has an hindex of 30, co-authored 59 publications receiving 5806 citations. Previous affiliations of Don J. Mahad include Cleveland Clinic Lerner Research Institute & Newcastle University.
Papers
More filters
Journal ArticleDOI
Glycolytic oligodendrocytes maintain myelin and long-term axonal integrity
Ursula Fünfschilling,Lotti Marianna Supplie,Don J. Mahad,Don J. Mahad,Susann Boretius,Aiman S. Saab,Julia M. Edgar,Bastian G. Brinkmann,Celia M. Kassmann,Iva D. Tzvetanova,Wiebke Möbius,Francisca Diaz,Dies Meijer,Ueli Suter,Bernd Hamprecht,Michael W. Sereda,Carlos T. Moraes,Jens Frahm,Sandra Goebbels,Klaus-Armin Nave +19 more
TL;DR: By in vivo magnetic resonance spectroscopy, brain lactate concentrations in mutants were increased compared with controls, but were detectable only in mice exposed to volatile anaesthetics, which indicates that aerobic glycolysis products derived from oligodendrocytes are rapidly metabolized within white matter tracts.
Journal ArticleDOI
Progressive multiple sclerosis: pathology and pathogenesis
TL;DR: Oxidative stress seems to be mainly driven by inflammation and oxidative burst in microglia; however, its effects might be amplified in patients with progressive MS by age-dependent iron accumulation in the brain and by mitochondrial gene deletions, triggered by the chronic inflammatory process.
Journal ArticleDOI
NADPH oxidase expression in active multiple sclerosis lesions in relation to oxidative tissue damage and mitochondrial injury
Marie Therese Fischer,Rakhi Sharma,Jamie L. Lim,Lukas Haider,Josa M. Frischer,Joost A. R. Drexhage,Don J. Mahad,Monika Bradl,Jack van Horssen,Hans Lassmann +9 more
TL;DR: The data suggest that the inflammation-associated oxidative burst in activated microglia and macrophages plays an important role in demyelination and free radical-mediated tissue injury in the pathogenesis of multiple sclerosis.
Journal ArticleDOI
The role of MCP-1 (CCL2) and CCR2 in multiple sclerosis and experimental autoimmune encephalomyelitis (EAE)
TL;DR: Evidence from descriptive, transgenic, knockout and neutralizing studies of experimental autoimmune encephalomyelitis (EAE) points towards a nonredundant role of CCL2 and CCR2 in the recruitment of inflammatory infiltrate into the CNS.
Journal ArticleDOI
Mitochondrial changes within axons in multiple sclerosis
Don J. Mahad,Iryna Ziabreva,Graham R. Campbell,Nichola Z. Lax,Katherine White,Peter S. Hanson,Hans Lassmann,Douglass M. Turnbull +7 more
TL;DR: In vitro studies show that inhibition of complex IV augments glutamate-mediated axonal injury (amyloid precursor protein and SMI32 reactivity), which has important implications for both axonal degeneration and dysfunction during the progressive stage of multiple sclerosis.