The two-phase model of the pathogenesis of multiple sclerosis (MS) is discussed in the aspect of inflammation and neurodegeneration processes. In the first phase, there are inflammation processes with frequent exacerbations and remissions and multiple lesions on MRI. An axonal lesion (neurodegeneration) is seen in this stage, even in the very beginning, i.e. in the stage of clinically isolated syndrome. The possibilities of treatment of neurodegenerative changes, in particular, with glatiramer acetate (GA) or copaxon, are reviewed. Copaxon induces a switch from Th1-cells to GA-specific Th2-lymphocyte production which can produce neurotrophic factors. Clinical and MRI data as well as experimental results supporting the neuroprotective effect of this drug are presented.