GFAP and Alzheimer disease: BV sPLA2 improved memory function, suppressed Aβ deposition, inhibited neuroinflammation and NF-κB activation through the downregulation of glial fibrillary acidic protein (GFAP), ionised calcium binding adaptor molecule 1 (IBA-1), inducible nitric oxide synthase (iNOS), COX-2, p-IκB-α, p50 and p65, and modulated Tregs infiltration through the upregulation of Foxp3 in a lipopolysaccharide (LPS)-induced AD mouse model brain.