In Aβ1–42-infused mice, the transplantation of P-MSCs, which are MSCs with anti-amyloidogenic and anti-neuroinflammatory effects, improved neuronal survival and neurogenesis and prevented memory deficiency.375 Overproduction of VEGF by BM-MSCs favored neovascularization and Aβ protein clearance, ultimately restoring memory and learning deficits in 2xTg-AD mice.376 Transplantation of human UC-MSCs into AD mice alleviated the rate of decline in memory and learning ability and improved the progression of disease in AD mice by reducing Aβ deposition.377. This evidence concerns the gene VEGFA and Alzheimer disease.