TLR4 and Alzheimer disease: A further study used LPS-stimulated mice to replicate pathological alterations in the initial stages of AD, revealing that GAS (100 mg/kg) suppressed TLR4/TRAF6/NF-κB pathway-related proteins expression, promoted the transformation of microglia from a pro-inflammatory to an anti-inflammatory phenotype, and mitigated neuroinflammation in hippocampal neurons, thereby improving the LPS-induced deficits in memory and learning (Wang et al., 2024).