Abstract: Alzheimer’s disease(AD) is a progressive neurodegenerative disease that seriously endangers the health of the elderly, with a complex pathogenesis. Neuroinflammation, amyloid-β peptide(Aβ) deposition, and excessive tau protein phosphorylation are its core pathological features, imposing a heavy burden on families and society. As the major immune cells in the central nervous system, the dysfunction of microglia is a key driving force for the occurrence and development of neuroinflammation in AD. Triggering receptor expressed on myeloid cells 2(TREM2) and the NOD-, LRR-, and pyrin domain-containing protein 3(NLRP3) inflammasome are the core molecules that regulate microglial activation and neuroinflammation. This paper systematically reviews the mechanisms of TREM2 and the NLRP3 inflammasome in neuroinflammation of AD, with a focus on their interactive regulatory relationship: TREM2 can regulate the phenotypic transformation of microglia through signaling pathways such as phosphatidylinositol 3-kinase(PI3K)/protein kinase B(AKT)/mammalian target of rapamycin(mTOR) and toll-like receptor 4(TLR4)/nuclear factor-kappa B(NF-κB), inhibit the activation of the NLRP3 inflammasome and the release of proinflammatory factors, and participate in Aβ clearance and neuronal protection. Abnormal activation of the NLRP3 inflammasome will exacerbate neuroinflammation and the pathological processes of AD by forming a vicious cycle of "inflammatory factor secretion-pathological damage" and can negatively regulate the TREM2 signaling pathway. Meanwhile, this paper summarizes the therapeutic strategies for AD targeting TREM2, the NLRP3 inflammasome, and their combined intervention, and analyzes the current progress and challenges in therapeutic research. This work provides a theoretical basis and research ideas for further clarifying the molecular regulatory mechanism of neuroinflammation in AD and developing efficient and safe targeted therapeutic drugs for AD.