Genetics

This post sets three recent studies at the intersection of MS genetics and metabolism against each other. It covers the summary data-based Mendelian randomization across 936 oxidative stress genes that identified TSFM with brain eQTL support, the Cell study tracking interferon-gamma through PSMB8 and PFKFB3 accumulation into neuronal glycolysis and ferroptosis, and the Nature study showing ATP-citrate lyase controlling astrocyte inflammatory memory through chromatin accessibility. It then argues that the three describe three distinct kinds of metabolic involvement rather than one pathway, that the gene with human inherited evidence has no mechanism attached while the mechanisms with experimental evidence have no reported population-level support, and that each design answers a question the others cannot.