Researchers from the University of British Columbia presented data from a study that aimed to define the role of nuclear receptor subfamily 1 group H member 3 (NR1H3) in the pathophysiological mechanisms that drive increased risk, severity and progression in multiple sclerosis (MS).

Researchers from Georgetown University presented data from a study that aimed to assess the intrinsic mechanisms by which myeloid cells regulate their activation states during remyelination and to identify new therapeutic targets for multiple sclerosis (MS).

Previous research has suggested that neurons in multiple sclerosis (MS) exhibit metabolic exhaustion, believed to be caused by chronic hyperexcitability, which can lead to neurodegeneration. Researchers from Heidelberg University and affiliated organizations aimed to investigate the role of nodal Kv7 (outward rectifying) and perinodal oligodendroglial Kir4.1 (inward rectifying) channels as potential therapeutic targets for neuroprotection through balancing of neuronal excitability caused by inflammatory demyelination.

Current therapies for multiple sclerosis (MS) focus on targeting immunomodulatory mechanisms...

It was previously demonstrated that the CNS-penetrant compound bryostatin-1 (bryo-1) exerts an immunomodulatory effect on myeloid-lineage innate immune cells in the periphery through its actions on protein kinase C (PKC). In a new study, researchers from Johns Hopkins University aimed to assess the potential of bryo-1 for the treatment of progressive multiple sclerosis (MS) by investigating its effect on remyelination.

Therapies for multiple sclerosis (MS) have been effective in relapse prevention but emerging data still show the continued disability progression independent of relapse activity (PIRA), characterized by the presence of ectopic B-cell follicles and active lesions with microglia cells, resulting in a smoldering central nervous system (CNS)-driven inflammation, tissue damage and disease progression.

Boston Immune Technologies and Therapeutics Inc. (BITT) has announced progress using its Domab platform. Two Domab CD40 antagonists, BITT-CD4D11 and BITT-CD4F10, have completed discovery and optimization and a final candidate is being selected for IND-enabling steps.