This was due to the low level of AdoMet in the brains of AD patients, which affected CBS activity and thus reduced the synthesis of H2S. In a severe AD model, H2S supply reduced Aβ deposition, hyperphosphorylation of p-APP (the precursor protein of Aβ) and Tau isoforms, and the inflammatory response to improve cognitive activity (52). This evidence concerns the gene MAPT and Alzheimer disease.