This study demonstrated that supplementation of a HFD with blueberry reduced indices of microglia activation and increased neuroplasticity, and these changes may underlie the protection against memory deficits in HFD-fed mice supplemented with blueberry.

No abstract

Previously it was demonstrated that 9 month old mice fed a high fat diet (HFD, Harlan, TD.06414, 60% calories from lard fat) for five months had impaired memory; however supplementation of the HFD with 4% blueberry (BB, freeze‐dried extract, U.S. Highbush Blueberry Council) reduced these memory deficits. The brains of these mice were dissected, homogenized, and assayed with ELISA for brain‐derived neurotrophic factor (BDNF), the inflammatory cytokine tumor necrosis factor (TNF)‐alpha, and were evaluated for oxidative stress by examining 4‐Hydroxynonenal (4‐HNE). There was a significant increase in hippocampal BDNF in the animals fed the HFD + BB (273±56 pg/ml/per mg of tissue) in comparison with the low fat diet (LFD, TD.08806, 10% calories from fat) and HFD‐fed animals without BB supplementation (44±3 and 46±2 pg/ml, respectively). There was also a trend suggesting that animals fed a LFD + BB had elevated BDNF levels (101±57 pg/ml). Greater levels of TNF‐alpha were found in the cerebral cortex of mice fed a HFD compared to mice fed a LFD, and there was a partial reduction of TNF‐alpha in mice fed HFD + BB. 4‐HNE was found to be elevated in the cortex of mice fed a HFD compared to the mice that had BB supplementation in the HFD. This study attempts to determine the pathways and molecules that HFD consumption modulates that may underlie the previously demonstrated memory impairment, and also to begin to elucidate the mechanisms by which blueberry supplementation mediates these changes. Supported by U.S. Highbush Blueberry Council