Genetics

This post sets four recent papers on MS metabolism against each other, one from each of three research lines plus a review. It covers the mitochondrial microprotein MOCCI, product of C15orf48, which sets whether glial activation resolves or persists and acts in both demyelination and remyelination in the cuprizone model; the four-cohort study showing smoking depletes bile acids and tryptophan metabolites with indolepropionate mediating about a fifth of smoking's effect on MS severity; the pooled analysis of four randomized trials in which strength exercise acutely raised a neuroprotective kynurenine pattern and 24 weeks of endurance exercise lowered a neurotoxic one; and the review placing all of it inside lymphocyte metabolic reprogramming. It closes on the tryptophan convergence between two of the studies and on where each design fails.