The professor of neurology at the University of Saskatchewan discussed his presentation at the 2022 CMSC Annual Meeting on using ribonucleoprotein A1 antibodies to drive neurodegeneration in multiple sclerosis. [WATCH TIME: 4 minutes]
WATCH TIME: 4 minutes
"As we add these A1 antibodies to that model, nerve cells A1 are misplaced and nerve cells die. Then we take primary nerve cells isolated from mouse brain and showed the same thing. Why is this important? We think that if we can get A1 back into the nucleus where it belongs, we will rescue nerve cells."
Despite the progress and expansion of improved disease-modifying therapies (DMTs), clinicians have few answers for the neurodegeneration found in patients with multiple sclerosis (MS). Both relapsing and progressive forms of the disease experience this decline to some extent, although its more pronounced in patients with progressive MS and thus has added to the struggle of designing effective DMTs.
At the 2022 Consortium of Multiple Sclerosis Centers (CMSC) Annual Meeting, June 1-4, in National Harbor, Maryland, a mouse model study looked at whether autoimmune-induced RNA binding protein (RBP) dysfunction contributes to mechanisms of neurodegeneration in MS. In the analysis, mice with experimental autoimmune encephalomyelitis (EAE) were treated with ribonucleoprotein A1 antibodies or saline and had spinal cords analyzed for markers of RBP dysfunction and neurodegeneration over a 21-day period following symptom onset.1
In EAE, A1 antibody treatment resulted in a 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 formation at days 15 and 21 (P <.01). To learn more about the results, NeurologyLive® sat down with senior investigator Michael Levin, MD, FAAN, FANA, professor of neurology, University of Saskatchewan. Levin discussed the research that led up to these results, as well as the next steps in expanding the findings.