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Although with a lower tumorigenic capacity than a chronic high-fat diet, a chronic high-carbohydrate diet promoted ADM and PanIN lesions with increased inflammation and fibrosis compared to a normal diet in Kras G12D/+ mice [54]
Exposure to environmental and cellular derived toxicants damages the brain directly and further exacerbates oxidative and inflammatory injury
The change induces difficulty in repairing ruptures of double-stranded DNA, increases ROS production, mitochondrial dysfunction, with concomitant oxidative stress and consequent cell apoptosis [10, 11]
Glutamate accumulation to micromolar levels [375] results in GluN2B-mediated NMDA receptor overactivation, Ca 2+ overload, and subsequent tau hyperphosphorylation and dendritic spine collapse [376], linking excitotoxicity to amyloidogenesis [28]
