Orla M. Finucane

TL;DR: This review will investigate obese AT biology, initiation of the inflammatory, and insulin resistant environment; and the mechanisms through which dietary anti-inflammatory components/functional nutrients may be beneficial.

TL;DR: The data suggest that activation of the inflammasome contributes to amyloid accumulation and to the deterioration of neuronal function in APP/PS1 mice and demonstrate that blocking assembly of theInflammation may prove to be a valuable strategy for attenuating changes that negatively impact on neuronal function.

TL;DR: In vitro, it is demonstrated that the MUFA oleic acid can impede ATP-induced IL-1β secretion from lipopolysaccharide- and SFA-primed cells in an AMPK-dependent manner and suggest that dietary MUFA can attenuate IL- 1β–mediated insulin resistance and adipose dysfunction despite obesity via the preservation of AMPK activity.

TL;DR: SFA represent metabolic triggers priming the inflammasome, promoting adipocyte inflammation/IR, suggesting direct effects of SFA on inflammaome activation via TLR4.

TL;DR: Analysis of microglia prepared from wildtype mice and from transgenic mice that overexpress amyloid precursor protein and presenilin 1 revealed genotype-related increases in glycolysis, accompanied by increased PFKFB3, and an increase in the expression of ferritin suggesting that increased intracellular iron concentration may drive the metabolic and/or inflammatory changes.