Gal-3 expression in the brain increased in an age-dependent manner.86,87 Functional studies showed that endogenous Aβ-oligomerisation was decreased in Gal-3 knockouts.86,87 Both studies showed that Gal-3 physically interacts with TREM2 a major risk factor for AD and Boza-Serrano et al showed that this interaction required the CRD of Gal-3.86 Gal-3 activation of microglia was TREM2-dependent.87 In 5xFAD/Gal-3KO brain slices, recombinant Gal-3 was shown to bind to TREM2+/Iba1+, but not TREM2−/Iba1+ microglia. This evidence concerns the gene AIF1 and Alzheimer disease.