Familial Alzheimer's disease and amyotrophic lateral sclerosis (ALS)‐associated mutations in presenilins and superoxide dismutase 1 confer ferroptosis vulnerability by inhibiting GPX4 expression through limiting LRP8‐mediated selenium uptake and impairing the NRF2 pathway and GSH synthesis, respectively.144, 145. Here, LRP8 is linked to amyotrophic lateral sclerosis.