Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system with presumed autoimmune etiology. Within the last years an important success has been achieved in understanding the pathophysiology of the disease and in making available effective therapeutic agents able to change the natural course of the disorder, particularly of its relapsing-remitting form. More recently, the advances made in understanding the biology of remyelination in MS opened a wide window of opportunity to design innovative therapeutic strategies that could really have an impact in reducing progressive accumulation of disability in MS and actually function as neuroprotectors and neuro regenerators. Here we provide an overview of the key target pathways and mechanisms that were identified in this field and that can provide smart targets for future pharmacological intervention Palavra F, et al. Remyelination in Multiple Sclerosis â How Close are We?.
The actual cause of multiple sclerosis is unknown and there is no hereditary role of multiple sclerosis revealed yet. But the role of certain gene in multiple sclerosis associated risk has been revealed. HLA-DRB1 associated mutations are considered as one of the strong candidate genes in development of multiple sclerosis. Role of a similar candidate gene IL7R gene is also being investigated.
Last date updated on June, 2014