In a D-galactose/aluminum chloride-induced model of Alzheimer’s disease, selenium nanoparticles-enriched L. casei (ATCC 393) administered for thirteen weeks significantly improved cognitive dysfunction and minimized β-amyloid aggregation, hyperphosphorylation of Tau protein, and prevented neuronal death by modulating the Akt/cAMP-response element binding protein/BDNF signaling pathway (502). The gene discussed is MAPT; the disease is early-onset autosomal dominant Alzheimer disease.