The results indicate that PEA treatment attenuated Aβ-induced astrocyte activation, as proven by its effects in reducing astrocyte hypertrophied cell bodies and thickened processes, along with the expression of glial fibrillary acidic protein (GFAP) and S100 calcium-binding protein B (S100B), two specific markers of astrocyte activity also linked to AD pathogenesis. Here, S100B is linked to Alzheimer disease.