It was reported that sulforaphane inhibits HDAC activity and increases histone-tail acetylation in 3×Tg-AD mice, thereby increasing BDNF levels and enhancing activation of the BDNF-TrkB signaling pathways, which might further facilitate neuronal differentiation and growth, promote survival of neurons, and induce synaptic plasticity and long-term potentiation [33]. This evidence concerns the gene BDNF and Alzheimer disease.