title: Excitotoxins, Mitochondrial and Redox Disturbances in Multiple Sclerosis.
abstract: Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). There is increasing evidence that MS is not only characterized by immune mediated inflammatory reactions, but also by neurodegenerative processes. There is cumulating evidence that neurodegenerative processes, for example mitochondrial dysfunction, oxidative stress, and glutamate (Glu) excitotoxicity, seem to play an important role in the pathogenesis of MS. The alteration of mitochondrial homeostasis leads to the formation of excitotoxins and redox disturbances. Mitochondrial dysfunction (energy disposal failure, apoptosis, etc.), redox disturbances (oxidative stress and enhanced reactive oxygen and nitrogen species production), and excitotoxicity (Glu mediated toxicity) may play an important role in the progression of the disease, causing axonal and neuronal damage. This review focuses on the mechanisms of mitochondrial dysfunction (including mitochondrial DNA (mtDNA) defects and mitochondrial structural/functional changes), oxidative stress (including reactive oxygen and nitric species), and excitotoxicity that are involved in MS and also discusses the potential targets and tools for therapeutic approaches in the future.
authors.affiliation: Department of Neurology, University of Szeged, 6725 Szeged, Hungary. rajda.cecilia@med.u-szeged.hu.
authors.forename: Cecilia
authors.initials: C
authors.lastname: Rajda
authors.affiliation: Department of Neurology, University of Szeged, 6725 Szeged, Hungary. pukoli.daniel@med.u-szeged.hu.|Department of Neurology, Vaszary Kolos Hospital, 2500 Esztergom, Hungary. pukoli.daniel@med.u-szeged.hu.
authors.forename: Dániel
authors.initials: D
authors.lastname: Pukoli
authors.affiliation: Department of Neurology, University of Szeged, 6725 Szeged, Hungary. bendzsu@gmail.com.
authors.forename: Zsuzsanna
authors.initials: Z
authors.lastname: Bende
authors.affiliation: Department of Neurology, University of Szeged, 6725 Szeged, Hungary. majlathzsofia@gmail.com.
authors.forename: Zsófia
authors.initials: Z
authors.lastname: Majláth
authors.affiliation: Department of Neurology, University of Szeged, 6725 Szeged, Hungary. vecsei.laszlo@med.u-szeged.hu.|MTA-SZTE Neuroscience Research Group, 6725 Szeged, Hungary. vecsei.laszlo@med.u-szeged.hu.
authors.forename: László
authors.initials: L
authors.lastname: Vécsei
mesh_terms: D000818:Animals; D015415:Biomarkers; D001812:Blood-Brain Barrier / Q000378:metabolism / Q000473:pathology; D004195:Disease Models, Animal; D018450:Disease Progression; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D008928:Mitochondria / Q000378:metabolism*; D009103:Multiple Sclerosis / Q000209:etiology / Q000378:metabolism* / Q000473:pathology / Q000628:therapy; D009498:Neurotoxins / Q000378:metabolism*; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D017470:Receptors, Glutamate / Q000378:metabolism
chemical_list: D015415:Biomarkers; D009498:Neurotoxins; D017470:Receptors, Glutamate; D018698:Glutamic Acid
keywords: biomarker; excitotoxin; glutamate; mitochondria; multiple sclerosis; neurodegeneration; oxidative stress