Genetics

This post covers three recent papers that ask which cells survive in MS rather than which fail, and how much a cell-level observation can be made to carry. It follows the Nature study finding complement factor H doing a non-canonical job inside neurons, restraining reactive oxygen species and lipid peroxidation at the endoplasmic reticulum, and unpacks the three subtractive controls behind that claim: domain mapping, independence from secretion, and survival without complement component C3. It then covers the Glia study of mice whose small-diameter axons persist a year without compact myelin, where proteomics pointed to 14-3-3 isoforms and two inhibitors confirmed them, and the myeloid framework separating what single-cell and spatial data can infer from what only origin-resolving methods can establish. It states plainly where metabolism is central and where it is not.