Dietary Supplementation with S-Adenosyl Methionine Delayed Amyloid-β and Tau Pathology in 3xTg-AD Mice

摘要: S-adenosyl methionine (SAM) contributes to multiple pathways in neuronal homeostasis, several of which are compromised age-related neurodegeneration and Alzheimer's disease. Dietary supplementation transgenic mice with SAM maintained acetylcholine levels, cognitive performance, oxidative buffering capacity, phosphatase activity, reduced aggression, calcium influx, endogenous PS-1 expression, γ-secretase levels amyloid-β (Aβ) phospho-tau. Herein, we examined whether or not could delay neuropathology 3xTg-AD mice, harbor mutant genes for human AβPP, tau. Mice received a standard AIN-76 diet without (100 mg/kg diet) 1 month commencing at 10 months age 3 12.5 age; were sacrificed Aβ tau 11 15.5 age, respectively. hippocampal intracellular AβPP/Aβ phospho-tau immunoreactivity similar extent both sampling intervals. Supplementation the number extracellular deposits by 80% (p < 0.01) after treatment but only 24% 0.34) treatment. As anticipated, neurofibrillary tangles observed these young ages; however, caspase-cleaved within Sarkosyl-insoluble preparations age. These limited analyses indicate that can modulate time course AD neuropathology, support further long-term analyses.