Due to the growth in aging populations, prevention for
cognitive decline and
dementia are in great demand. We previously demonstrated that the consumption of iso-α-
acids (IAA), the hop-derived bitter compounds in beer, prevents
inflammation and
Alzheimer's disease pathology in model mice. However, the effects of iso-α-
acids on
inflammation induced by other agents aside from
amyloid β have not been investigated. In this study, we demonstrated that the consumption of iso-α-
acids suppressed microglial
inflammation in the frontal cortex of rTg4510
tauopathy mice. In addition, the levels of inflammatory
cytokines and
chemokines, including IL-1β and MIP-1β, in the frontal cortex of rTg4510 mice were greater than those of wild-type mice, and were reduced in rTg4510 mice fed with iso-α-
acids. Flow cytometry analysis demonstrated that the expression of cells producing CD86, CD68, TSPO, MIP-1α, TNF-α, and IL-1β in microglia was increased in rTg4510 mice compared with wild-type mice. Furthermore, the expression of CD86- and MIP-1α-producing cells was reduced in rTg4510 mice administered with iso-α-
acids. Moreover, the consumption of iso-α-
acids reduced the levels of phosphorylated tau in the frontal cortex. Collectively, these results suggest that the consumption of iso-α-
acids prevents the
inflammation induced in
tauopathy mice. Thus, iso-α-
acids may help in preventing
inflammation-related
brain disorders.