LRP8 and Alzheimer disease: Presenilins, which are depleted due to mutations in familial forms of AD, have been shown to suppress ferroptosis promotion and more extensively suppress GPX4 expression by regulating selenium supply to the cells via selenoprotein P, which delivers it to the low-density lipoprotein receptor-related protein 8 (LRP8) which, when knocked out in mice, reduces brain selenium by more than 50% and results in severe neurodegeneration [210].