The capacity of melatonin, both pineal and locally, to upregulate mitophagy as well as to suppress oxidative stress and the NLRP3 inflammasome in Alzheimer’s disease and Alzheimer’s disease models [151] would indicate that melatonin upregulates miR-138, thereby contributing to NLRP3, CTLA-4 and PD-1 suppression, with relevance to aging-associated changes in immune responsivity (see Figure 7). This evidence concerns the gene CTLA4 and early-onset autosomal dominant Alzheimer disease.