In summary, our results are consistent with published observations that depletion of gut bacteria attenuates microglial inflammatory activation and Aβ pathology in the brain of APP-transgenic mice; however, we further elucidated the possible mechanisms mediating the gut-brain axis in AD pathogenesis: 1) depletion of gut bacteria reduces peripherally circulating Il-17a-expressing T lymphocytes and translocation ofbacterial components from the gut to the brain. Here, IL17A is linked to Alzheimer disease.