Alzheimer’s disease (AD) is an acquired neurodegenerative disease that leads to the loss of cognitive functions such as memory and affects a person’s ability to perform everyday tasks. The pathogenesis of this disease is not yet fully understood and requires more research to find effective treatments. A growing body of evidence indicates that dysbiosis of the microbiota may promote the appearance of AD. The present study seeks to identify gut microbiota signatures that may modulate AD pathogenesis. My colleagues performed 66-day fecal microbiota transplantation (FMT, 1x/7 days) in APP(Swe), PS1(M146V), and Tau(P301L) triple transgenic mice from fecal bacteria isolated from human participants with different risk factors for AD. I then participated in the analysis of murine behavioral tests and the quantification of AD-associated biomarkers such as amyloid-beta and phosphorylated tau protein. My results indicate that FMT does not induce significant behavioral changes. In contrast, FMT combined with antibiotic and gastric acid suppressant administration significantly reduces amyloid-beta 42 levels in the brain and gut. Future characterization of the gut microbiota of these mice by 16s sequencing will assess whether a change in the bacterial signature is present in antibiotic- treated mice and may be associated with decreased amyloid-beta 42 levels.