Shifting Focus From Relapses to Neurodegeneration in MS: Michael Levin, MD, FAAN, FANA

WATCH TIME: 4 minutes

At the 2022 Consortium of Multiple Sclerosis Centers (CMSC) Annual Meeting, June 1-4, at National Harbor, Maryland, a group of investigators presented a mouse model study aimed at understanding the contribution of autoimmune-induced RNA binding protein (RBP) dysfunction to mechanisms of neurodegeneration in MS. Previously, the team showed that RBP heterogenous nuclear ribonucleoprotein A1 antibodies exacerbate A1 dysfunction and neurodegeneration; however, it was unclear whether A1 dysfunction triggers or occurs as a result from neurodegeneration.

The analysis featured mice with experimental autoimmune encephalomyelitis (EAE) who were treated with either A1 antibodies or saline and had spinal cords analyzed at 7, 15, and 21 days after symptom onset.1 At the conclusion of the study, A1 antibody treatment resulted in statistically significant increase in A1 mislocalization at days 7 and 15 (P <.05), alteration in RNA expression at day 15, and increase in stress granule formulation at days 15 and 21 (P <.01). Additionally, RNA sequencing revealed enriched pathways related to regulation of neuronal projects, cell stress, and programmed cell death.

Senior investigator Michael Levin, MD, FAAN, FANA, believes that the time to hone in on neurodegeneration is now, citing that the disease-modifying therapies (DMTs) aimed at targeting relapses have vastly improved. Levin, professor of neurology at the University of Saskatchewan, sat down with NeurologyLive^® for an interview to discuss the potential of an A1 antibody treatment and who it would be best suited for if it came to fruition. He also provided context on the progress of DMTs and the needs for patients with progressive MS.

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REFERENCE
1. Libner CD, Salapa HE, Levin M. Ribonucleoprotein autoimmunity drives neurodegeneration in multiple sclerosis models. Presented at: CMSC Annual Meeting; June 1-4, 2022; National Harbor, MD. Whitaker Research Track.