Опубликована: Апрель 23, 2025

Alzheimer's disease (AD) is characterized by the buildup of extracellular aggregated amyloid-β (Aβ) peptides, following sequential enzymatic cleavage amyloid precursor protein (APP), along with intraneuronal accumulation hyperphosphorylated Tau proteins (pTau) and subsequent neuronal loss. Despite extensive research, precise mechanisms underlying Aβ, Tau-mediated neurodegeneration remain elusive. Inhibiting aggregation has been a primary focus for mitigating toxicity. The gut-brain axis potential factor in AD progression, evidence suggesting that gut-resident bacteria may produce contribute to host aggregation. Altered gut microbial diversity also observed individuals AD. Probiotics have emerged as promising preventative measure against cognitive decline AD, several in vivo clinical trials demonstrating efficacy select bacterial strains slowing progression. However, these studies lack direct molecular on effects probiotics Aβ kinetic. In this study, we conducted bioinformatic physicochemical assessments, including docking derived from 13 probiotic Tau, identifying four predicted efficiently inhibit Kinetic confirmed both formulation its supernatant significantly inhibited conversion monomeric into forms. To explore bioavailability, administered healthy detected presence stool samples, survival through gastrointestinal tract. These findings suggest specific serve therapeutic candidates targeting aggregation, further warranted assess their utility

Язык: Английский