Further analysis demonstrated that METTL3 ablation in monocyte-derived macrophages attenuated the m6A modification in Dnmt3a mRNAs and subsequently impaired the translation of DNMT3A and ATAT1 expression and acetylation of tubulin, which enhanced the migration of monocyte-derived macrophages, accelerated the clearance of Aβ and alleviated AD symptoms. This evidence concerns the gene DNMT3A and Alzheimer disease.