Our data show that L41 treatment in APP/PS1 mice promotes a moderate reduction of the amyloid load, which may be explained by the induction of an activated microglia phenotype expressing increased levels of TREM2 (triggering receptor expressed on myeloid cells 2) and IDE (insulin degrading enzyme), two microglial proteins that have been demonstrated to regulate Aβ deposition in AD mouse models [12, 14, 48]. The gene discussed is PSEN1; the disease is Alzheimer disease.