After four months, the researchers ascertained improved spatial learning and memory deficits, reduced neuron damage, reduced synaptic protein loss, the inhibition of both tau protein pathology and Aβ aggregation, the activation of brain-derived neurotrophic factor, BDNF, and the family of proto-oncogenic tyrosine kinases genes, Src-mediated TrkB signaling, and increased MT3 and ZnT3 levels, so SELENOP-H restored Zn2+ homeostasis in the mice model of AD [111]. The gene discussed is BDNF; the disease is Alzheimer disease.