Alzheimer's disease (AD) is a neurodegenerative disorder with insidious onset and gradual development. Its symptoms include loss of memories, impaired language, reduced spatial perception, mood swings, and reduced ability to perform calculations and abstract thinking. AD is the most common type of dementia in the aged. Around the globe, more than 40 million people suffer from AD, and the number continues to rise. At present, there are many hypotheses about the pathogenesis of Alzheimer's disease, but the specific pathogenesis is not clear. Currently, due to unclear pathogenesis, this disease has no specific treatment methods, mainly symptomatic treatment and supportive treatment. Nowadays, most of the treatments being studied focus on reducing levels of neurotoxic Aβ and Tau. However, these therapeutic targets appear to be secondary and not causally related to the development of AD. Microglia, as one of the most significant immune cells in the central nervous system (CNS) has shown considerable clinical efficacy against neurodegenerative diseases. Furthermore, one of the causes of AD progression also includes neuroinflammation mediated by malfunctioning microglia cells. Microglia may exhibit great therapeutic benefits in treating AD. There are currently three approaches to ameliorate pathological changes in AD patients through microglia: modifying microglia to reduce neurological damage caused by dysfunction, targeting microglia immune receptors to improve their immune response, and targeting microglia-mediated inflammatory response to reduce inflammatory damage.