In the context of AD pathology, sodium butyrate supplementation selectively suppressed class I HDACs (HDAC1, HDAC2, HDAC3, HDAC8) in the hippocampal region, which significantly ameliorated memory formation and cognitive performance in a mouse model of AD (47), thereby underscoring the role of SCFAs in maintaining neuroplasticity via epigenetic reprogramming. This evidence concerns the gene HDAC3 and Alzheimer disease.