TB administration was purposely initiated at 6 months of age in 3×Tg mice, which corresponds to early-stage development of progressive amyloid and tau pathologies.11 Importantly, TB administration prevented the age-related decline in total butyrate-producing families and cecal butyrate levels that significantly correlated with the attenuation of neuropathological and cognitive changes associated with AD pathogenesis. This evidence concerns the gene MAPT and amyloidosis.