Possible Interaction: Selenomethionine and Uridine Triacetate

“In previous studies, we have reported that selenomethionine (Se-Met), a major form of selenium in animals and humans with significant antioxidant capacity, can reduce both amyloid-β (Aβ) deposition and tau hyperphosphorylation in a triple transgenic mouse model of AD.”

“ Selenomethionine (Se-Met), a major bioactive form of selenium (Se) in organisms with significant antioxidant capacity, reduced the levels of total tau and hyperphosphorylated tau and ameliorated cognitive deficits in younger triple transgenic AD (3xTg-AD) mice.”

“Thus, our results demonstrate for the first time that Se-Met mitigates cognitive decline by targeting both the hyperphosphorylation of tau and the autophagic clearance of tau in AD mice.”

“We find that selenomethionine promotes the initiation of autophagy via the AMPK–mTOR pathway and enhances autophagic flux, thereby facilitating tau clearance in vivo and in vitro.”

“… Se-Met effectively decreased the production and deposition of Aβ by inhibiting β-site amyloid … (BACE1)-regulated amyloid precursor protein (APP) processing and reduced the level of total tau and phosphorylated tau, which depended on depressing the activity and … kinase-3β (GSK-3β) and cyclin-dependent kinase 5 (CDK5).”