Platelets provide a bounty of potential targets for therapy in multiple sclerosis.

Multiple sclerosis (MS) and related demyelinating conditions like neuromyelitis optica are mediated via migration of leukocytes and monocytes from the peripheral circulation. This is particularly relevant in the initial phases of disease that manifests clinically with relapses and remission and dominates the pace of the evolution of these chronic diseases in the first decade. The most effective approved therapeutic approach for relapsing remitting MS, Natalizumab, blocks lymphocyte migration into the brain by targeting a4 integrin.1 Scant attention has been given to platelets in the pathophysiology of these diseases. And yet there have been hints that platelets play an important role in MS. For instance, an early study of MS lesions using gene microarrays indicated that glycoprotein IIb/IIIa was highly expressed in MS lesions and, surprisingly, particularly in the more chronic stages of the disease.2 Leukocyte–platelet interactions are mediated by 4 integrin, although 2, 5, and 6 are the primary integrins on platelets themselves.3