In mature oligodendroglia, hyperactivation of Drp1 inhibited hexokinase 1 leading to glycolytic defects that trigger NLRP3 inflammasome in AD models, whereas knockout of Drp1 corrected glycolytic defect, decreased activation of NLRP3 inflammasome, decreased myelin and axonal loss, and also enhanced cognitive function in AD models (Zhang et al. 2020a). This evidence concerns the gene HK1 and Alzheimer disease.