The involvement of S100B in AD is one such example: in late disease stages when it is overexpressed and secreted by astrocytes, S100B acts as a pro-inflammatory cytokine that promotes gliosis and aggravates neuroinflammation as a response to the accumulation of amyloid beta deposits [11]; however, at earlier inflammatory stages, when the relative levels of Aβ42 and S100B are still increasing, S100B exerts a protective chaperone-like activity engaging in interactions with Aβ42 that inhibit its aggregation and mitigate amyloid toxicity [12,13]. This evidence concerns the gene S100B and Alzheimer disease.