Metformin, monoacylglycerol lipase expression, cognition and emotion recognition in people with multiple sclerosis and comorbid type II diabetes: A case-control study

BackgroundDiabetes (DM), a common comorbidity, results in poorer cognition in people with multiple sclerosis (PwMS). Metformin may be a treatment option given cognitive benefits. Metformin represses monoacylglycerol lipase (Mgll), accompanied by improvements in cognition in animals. AimsTo determine 1) whether metformin represses Mgll in humans, 2) if Mgll correlates with cognition/emotion recognition, and 3) if cognition differs between groups. MethodsA convenience sample of seventeen PwMS and DM on metformin, 4 with MS and DM not on metformin, 10 with MS, and 21 healthy controls completed BICAMS and measures of premorbid ability, emotion recognition, mood and fatigue. Blood draw established Mgll levels. T-tests determined group differences in Mgll. Correlational analyses examined if Mgll correlated with cognition. ANCOVA evaluated differences in cognition/emotion recognition. ResultsGiven small samples, we combined groups to determine if metformin impacted Mgll regardless of diabetes status. Significant differences in Mgll (t = -2.07, p = .05), suggested that metformin suppresses Mgll. No relationship was found between Mgll and cognition/emotion recognition. Differences were found between PwMS and DM compared to controls in verbal learning (F = 5.85, p = .02) and memory (F = 5.62, p = .02). ConclusionsMetformin suppresses Mgll in humans suggesting metformin be evaluated as a potential MS treatment. Mgll did not correlate with cognition possibly due to sample size or methodology. Combined impact of MS and DM negatively impacts cognition, supporting literature demonstrating that vascular comorbidity increases risk of cognitive dysfunction. Findings support pursuing clinical trials evaluating metformin efficacy.