The main findings of the current study were that the long-term oral administration of ALA may relieve Aβ-induced glial cell-mediated neuroinflammation, apoptotic cell death, and synaptic dysfunction in a mouse model of Alzheimer’s disease (AD) by regulating TLR4, p-JNK, p-NF-kB, and p65 (Ser536) expression alongside the release of other inflammatory cytokines. Here, TLR4 is linked to early-onset autosomal dominant Alzheimer disease.