Although both peptides use FPR2 to induce migration and activation of monocytic phagocytes in the brain, Aβ42 and humanin display divergent roles in the development of Alzheimer’s disease: Aβ42 is a major cause of fibrillary formation and deposition in brain of AD patients [119,120], whereas humanin is neuroprotective on the contrary [121]. This evidence concerns the gene MT-RNR2 and early-onset autosomal dominant Alzheimer disease.