Taking this a step further, they interrupted this loop by inhibiting Pkm2 pharmaceutically or knocking out Pkm2 genetically, with an observation of compensatory expression of Pkm1 and a metabolic transition from glycolysis toward oxidative phosphorylation (OXPHOS), which eventually reduced Aβ burden and improved spatial learning and memory in AD mouse models (Pan et al., 2022). Here, PKM is linked to Alzheimer disease.