Multiple sclerosis (MS) progression is assumed to be driven by a central nervous system (CNS)-intrinsic inflammatory interplay of chronically activated CNS-resident cells and CNS-trapped hematopoietic immune cells.

This process substantially differs from MS relapse biology, and, accordingly, all agents designed to control relapses basically failed to control MS progression independent of acute inflammation.

New targets within the CNS driving MS progression have to be discovered and harnessed therapeutically.

Inhibition of Bruton's tyrosine kinase (BTK) may be one promising approach to control MS progression. BTK is centrally involved in the activation of immune cells such as B cells, but also in the chronic activation of microglia.