In APP/PS1 mice, a commonly used animal model of AD, which overexpresses the APP and presenilin 1 (PS1), the researcher attests that iron accumulation can drive microglia to switch to a glycolytic metabolic, thereby reducing the capacity to phagocytose Aβ, ultimately leading to Aβ accumulation (McIntosh et al., 2019). This evidence concerns the gene PSEN1 and Alzheimer disease.