Thus, it is essential and logical to determine whether constant restoration or increase in PITRM1 expression and function to maintain mitochondrial integrity in older AD mice by degrading and clearing toxic metabolites such as mitochondrial Aβ persistently protects against age‐ and Aβ‐mediated mitochondrial, synaptic, and cognitive perturbation. Here, PITRM1 is linked to Alzheimer disease.