Multiple sclerosis (MS) is the most common disabling neurological disease in 
young adults characterized by recurrent relapses and / or progression that are 
attributable to multifocal inflammation, demyelination and axonal pathology 
within the central nervous system. Currently approved disease-modifying 
treatments achieve their effects primarily by blocking the proinflammatory 
response in a nonspecific manner. Their limited clinical efficacy urges a more 
differentiated and specific therapeutic approach. Advances in understanding the 
pathophysiology of MS and appreciation of the contribution of neurodegenerative 
processes to disease pathology have led to promising therapeutic approaches at 
different points along the MS disease pathway: (i) monoclonal antibody therapy 
has provided the opportunity to rationally direct the therapeutic intervention 
by specifically targeting mechanisms of the immune system such as CD52 
(alemtuzumab), CD25 (daclizumab), VLA-4 (natalizumab) and CD20 (rituximab); (ii) 
novel oral immunomodulating agents have shown to prevent lymphocyte 
recirculation from lymphoid organs such as fingolimod (FTY720); (iii) blocking 
of intracellular signaling cascades or ion channels at the cell-surface can 
protect axons from degeneration and restore axonal function in experimental 
settings; (iv) neuroprotective agents and stem cell therapy are able to promote 
remyelination and axonal regeneration in vitro. Despite the tremendous efforts 
undertaken, a better understanding of the sequential evolution of the MS lesion 
and the development of clinical surrogate markers, which allow to define subsets 
of patients with different forms of underlying pathogenesis, is necessary. This 
will pave the way for an optimized treatment approach, which will likely need 
both to target inflammation and to focus on promotion of neuroprotection and 
repair.