Alzheimer's disease (AD) is the most prevalent neurodegenerative disease without effective treatments. Extracellular amyloid plaques, neurofibrillary tangles, neuroinflammation, and neuronal loss are the characteristics of AD neuropathology. Amyloid β protein (Aβ), the major component of amyloid plaques, is produced through the sequential cleavage of the amyloid precursor protein (APP) by β-secretase BACE1 and γ-secretase. Dysregulation of APP, BACE1, and γ-secretase increases Aβ generation while dysfunction of microglia reduces Aβ clearance, contributing to Aβ deposition. The increase in Aβ deposition simultaneously activates microglia, promoting the secretion of a large number of pro-inflammatory cytokines. Dysregulation of gut microbiota and their metabolites plays a pivotal role in AD pathogenesis. Among the metabolites, butyrate has beneficial effects on AD. Increasing the bioavailability of butyrate is critical for its clinical application. To achieve consistent supplementation of butyrate, we have developed a strain of engineered butyrate-producing Saccharomyces cerevisiae (J17), a yeast probiotic, which may mitigate AD phenotypes by the synergistic effect of butyrate supplementation and probiotic function of the chassis.