In early-stage AD, Gal-3 is upregulated in endothelial cells (ECs), promoting endothelial dysfunction and the endothelial-to-mesenchymal transition, thereby fostering a pro-inflammatory microenvironment, as observed in vascular disorders linked to AD, such as arterial hypertension and vascular inflammation [14–16]. This evidence concerns the gene LGALS3 and Alzheimer disease.