A growing body of evidence indicates a substantial role of the immune system and inflammation in the pathogenesis of Alzheimer’s disease (AD). In the current study, we investigated the effect of maternal immune activation (MIA) on AD-resembling pathological alterations in 12-month-old offspring. We also aimed to analyze whether inhibition of bromodomain and extraterminal domain (BET) proteins, the readers of the histone acetylation code, might impact these changes. In our study, we injected a viral mimetic polyinosinic-polycytidylic acid (PIC) at gestation day 17 to evoke MIA in wild-type mice C57BL6/J. An inhibitor of BET proteins, OTX-015, was administered orally to 12-month-old offspring males for two weeks. Then behavioral, genetic (qPCR), and immunochemical (ELISA, WB) analysis was performed. Our results demonstrated that MIA resulted in several molecular alterations in aged offspring. We detected an increased expression of App (qPCR) and level of amyloid-β (ELISA), but the level and phosphorylation of tau protein were not changed (WB). Also, mRNA levels of selected microglia activation markers, like Il6 and Nos2, were increased in the MIA group. Those changes significantly worsen the memory performance in MIA animals, as observed in a novel object recognition test. OTX-015 treatment reversed the memory loss and prevented the amyloid-β release but did not affect the expression of inflammatory genes or amyloidogenesis-related genes. Our results demonstrated that inhibition of BET proteins may offer an effective strategy for attenuating the neuropathological alterations evoked by prenatal infections.Funding: Narodowe Centrum Nauki, grant 2018/31/B/NZ4/01379