In our attempt to investigate the molecular mechanisms by which KAJD inhibits the production of Th2 cytokines, we found that KAJD dramatically downregulates IL-4 and IL-6 mRNA expressions and inhibits the MAPK (p38, ERK, and JNK) pathways in immune cells, such as murine splenocytes and human mast cells stimulated with LPS, indicating that KAJD alleviates several AD symptoms by controlling the transcriptional expression of Th2 cytokines. Here, IL4 is linked to Alzheimer disease.