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Publication : Iso-α-Acids, Bitter Components in Beer, Suppress Inflammatory Responses and Attenuate Neural Hyperactivation in the Hippocampus.

First Author  Ano Y Year  2019
Journal  Front Pharmacol Volume  10
Pages  81 PubMed ID  30804789
Mgi Jnum  J:281381 Mgi Id  MGI:6377805
Doi  10.3389/fphar.2019.00081 Citation  Ano Y, et al. (2019) Iso-alpha-Acids, Bitter Components in Beer, Suppress Inflammatory Responses and Attenuate Neural Hyperactivation in the Hippocampus. Front Pharmacol 10:81
abstractText  Due to the growth in aging populations worldwide, prevention and therapy for age-related cognitive decline and dementia are in great demand. We previously demonstrated that long-term intake of iso-alpha-acids, which are hop-derived bitter compounds found in beer, prevent Alzheimer's pathology in a rodent model. On the other hand, the effects of iso-alpha-acids on neural activity in Alzheimer's disease model mice have not been investigated. Here, we demonstrated that short-term intake of iso-alpha-acids suppresses inflammation in the hippocampus and improves memory impairment even after disease onset. Importantly, we demonstrated that short-term administration of iso-alpha-acids attenuated the neural hyperactivation in hippocampus. In 6-month-old 5 x FAD mice exhibiting hippocampus inflammation and memory impairment, oral administration of iso-alpha-acids for 7 days reduced inflammatory cytokines, including MIP-1alpha and soluble Abeta and improved object memory in the novel object recognition test. In 12-month-old J20 mice, intake of iso-alpha-acids for 7 days also suppressed inflammatory cytokines and soluble Abeta in the brain. Manganese-enhanced magnetic resonance imaging (MEMRI) of hippocampi of J20 mice showed increased manganese compared with wild type mice, but iso-alpha-acids canceled this increased MEMRI signal in J20 mice, particularly in the hippocampus CA1 and CA3 region. Taken together, these findings suggest that short-term intake of iso-alpha-acids can suppress hippocampus inflammation even after disease onset and improve hyper neural activity in Alzheimer's disease model mice.
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