title: Effects of glatiramer acetate and interferon-beta on neurodegeneration in a model of multiple sclerosis: a comparative study.
abstract: Axonal destruction and neuronal loss occur early during multiple sclerosis (MS), an autoimmune inflammatory central nervous system disease that frequently manifests with acute optic neuritis. Glatiramer acetate (GA) and interferon-beta-1b (IFN-beta-1b) are two immunomodulatory agents that have been shown to decrease the frequency of MS relapses. However, the question of whether these substances can slow neurodegeneration in MS patients is the subject of controversy. In a rat model of experimental autoimmune encephalomyelitis, we investigated the effects of GA and IFN-beta-1b on the survival of retinal ganglion cells (RGCs), the neurons that form the axons of the optic nerve. For each substance, therapy was started 14 days before immunization, on the day of immunization, or on the day of clinical disease onset. After myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis became clinically manifest, optic neuritis was monitored by recording visual evoked potentials. The function of RGCs was measured by electroretinograms. Although early GA or IFN-beta-1b treatment showed benefit on disease activity, only treatment with GA exerted protective effects on RGCs, as revealed by measuring neurodegeneration and neuronal function. Furthermore, we demonstrate that this GA-induced neuroprotection does not exclusively depend on the reduction of inflammatory infiltrates within the optic nerve.
authors.affiliation: Neurologische Universitätsklinik, Robert-Koch-Str. 40, D-37075 Göttingen, Germany. kmaier@gwdg.de
authors.forename: Katharina
authors.initials: K
authors.lastname: Maier
authors.forename: Antje V
authors.initials: AV
authors.lastname: Kuhnert
authors.forename: Naimeh
authors.initials: N
authors.lastname: Taheri
authors.forename: Muriel B
authors.initials: MB
authors.lastname: Sättler
authors.forename: Maria K
authors.initials: MK
authors.lastname: Storch
authors.forename: Sarah K
authors.initials: SK
authors.lastname: Williams
authors.forename: Mathias
authors.initials: M
authors.lastname: Bähr
authors.forename: Ricarda
authors.initials: R
authors.lastname: Diem
mesh_terms: D000818:Animals; D001369:Axons / Q000473:pathology; D002470:Cell Survival; D004596:Electroretinography; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000473:pathology / Q000517:prevention & control*; D005074:Evoked Potentials, Visual; D005260:Female; D000068717:Glatiramer Acetate; D000068576:Interferon beta-1b; D016899:Interferon-beta / Q000627:therapeutic use*; D009103:Multiple Sclerosis / Q000473:pathology / Q000517:prevention & control*; D009186:Myelin Sheath / Q000473:pathology; D019636:Neurodegenerative Diseases / Q000517:prevention & control; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D009900:Optic Nerve / Q000187:drug effects / Q000473:pathology; D009902:Optic Neuritis / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control; D010455:Peptides / Q000627:therapeutic use*; D051381:Rats; D011914:Rats, Inbred BN; D012165:Retinal Ganglion Cells / Q000187:drug effects* / Q000473:pathology
chemical_list: D018696:Neuroprotective Agents; D010455:Peptides; D000068576:Interferon beta-1b; D000068717:Glatiramer Acetate; D016899:Interferon-beta