Page last updated: January 10, 2017
Iso-α-acids, bitter components of beer prevent inflammation and cognitive decline induced in a mouse model of Alzheimer’s disease

Alongside the rapid growth in aging populations worldwide, prevention and therapy for age-related memory decline and dementia are in great demand to maintain a long healthy life.

A study found that iso-α-acids, hop-derived bitter compounds in beer, enhance microglial phagocytosis and suppress inflammation via activation of the peroxisome proliferator-activated receptor (PPAR-γ).

In normal mice, oral administration of iso-α-acids led to a significant increase both in CD11b and CD206 double-positive anti-inflammatory type microglia (P<0.05) and in microglial phagocytosis in the brain. In Alzheimer’s model 5xFAD mice, oral administration of iso-α-acids resulted in a 21% reduction in amyloid β (Aβ) in the cerebral cortex as observed by immunohistochemical analysis, a significant reduction in inflammatory cytokines such as interleukin 1β (IL-1β) and chemokines including macrophage inflammatory protein-1α (MIP-1α) in the cerebral cortex (P<0.05), and a significant improvement in a novel object recognition test (P<0.05), as compared with control-fed 5xFAD mice.

The differences in iso-α-acid-fed mice were due to the induction of microglia to an anti-inflammatory phenotype. The present study is the first to report that Aβ deposition and inflammation are suppressed in a mouse model of Alzheimer’s disease by a single component, iso-α-acids, via the regulation of microglial activation. The suppression of neuro inflammation and improvement in cognitive function suggests that iso-α-acids contained in beer may be useful for the prevention of dementia.

Source: Iso-α-acids, bitter components of beer, prevent inflammation and cognitive decline induced in a mouse model of Alzheimer’s disease. Y Ano, A Dhata, Y Taniguchi, A Hoshi, K Uchida, A Takashima and H Nakayama. The Journal of Biological Chemistry, first published 13 Jan 2017.

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