Due to the growth in aging populations worldwide, prevention and therapy for age-related cognitive decline and dementia are in great demand. A team of researchers previously demonstrated that long-term intake of iso-α-acids, which are hop-derived bitter compounds found in beer, prevent Alzheimer’s pathology in a rodent model.
The effects of iso-α-acids on neural activity in Alzheimer’s disease model mice have not, however, been investigated.
In a study published in the journal Frontiers in Pharmacology, the researchers demonstrated
that short-term intake of iso-α-acids suppresses inflammation in the hippocampus and improves memory impairment even after disease onset.
Importantly, they demonstrated that short-term administration of iso-α-acids attenuated the neural hyperactivation in hippocampus. In 6-month-old 5 Å~ FAD mice exhibiting hippocampus inflammation and memory impairment, oral administration of iso-α-acids for 7 days reduced inflammatory cytokines, including MIP-1α and soluble Aβ and improved object memory in the novel object recognition test. In 12-month-old J20 mice, intake of iso-α- acids for 7 days also suppressed inflammatory cytokines and soluble Aβ in the brain. Manganese enhanced magnetic resonance imaging (MEMRI) of hippocampi of J20 mice showed increased manganese compared with wild type mice, but iso-α-acids cancelled 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-α-acids can suppress hippocampus inflammation even after disease onset and improve hyper neural activity in Alzheimer’s disease model mice.
Source: Iso-α-Acids, bitter components in beer, suppress inflammatory responses and attenuate neural hyperactivation in the hippocampus. Ano Y, Yoshikawa M, Takaichi Y, Michikawa M, Uchida K, Nakayama H, Takashima A. Front Pharmacol. 2019 Feb 11;10:81. eCollection 2019.