The gut microbiome has been linked to neurodegenerative diseases, including Alzheimer’s disease (AD), in both humans and mouse models. There is potential for the use of probiotics to ameliorate AD, but they have not been specifically designed for AD treatment. Previous studies have shown that AD mice supplemented with short-chain fatty acids (SCFAs), including butyrate, had decreased Aβ deposition and tau hyperphosphorylation. Additionally, patients with AD have been found to have lower levels of butyrate-producing bacteria in their microbiome compared to healthy controls. Faecalibacterium prausnitzii​, Blautia faecis​, and Roseburia intestinalis​ are high butyrate producers and we found that these bacteria also produce metabolites that may have neuroprotective effects in neurodegenerative diseases. In this study, 5-month old male APP/PS1 mice were orally gavaged with the TriAD probiotic, a mix of Faecalibacterium prausnitzii​, Blautia faecis​, and Roseburia intestinalis, twice per week for 8 weeks with weekly microbiome sampling. After 8 weeks, the ileum, colon, lymph nodes, and brains were harvested. Preliminary results show a decrease in Aβ plaque number in the TriAD-treated APP/PS1 mice. TriAD treatment reduced Tbet+ γδ and CD8 T cells in the spleen, and reduced Gal3+ CD4 and CD8 T cells in the spleen and mesenteric lymph nodes of APP/PS1 mice. TriAD treatment reduced TNFα, IFNγ, and Granzyme B+ γδ T cells in the mesenteric lymph nodes of APP/PS1 mice. Studies to assess colonization of the TriAD probiotic, changes in SCFA production, synaptogenesis and neurogenesis in the brain, and microglial activation levels are currently ongoing. Future studies include determining sex-specific effects by repeating studies in female mice and examining cognitive changes through behavioral studies. Taken together, these findings suggest that our TriAD probiotic can ameliorate AD pathogenesis by lowering systemic inflammation and through the production of beneficial metabolites.