By inhibiting the expression of HDACs, VPA not only reduced the expression of Aβ42 in the AD cell model but also significantly impaired the deposition of Aβ in the cerebral cortex, hippocampus and entorhinal cortex (Fig. 10, Additional file 1: Fig. S9) and improved the cognitive function of APP/PSEN1 transgenic mice (Figs. 5, 6 and 7). This evidence concerns the gene PSEN1 and Alzheimer disease.