The lines of evidence presented above suggest that brain pro-inflammatory events associated with S100B-dependent glial activation in close proximity to β-amyloid plaques lead to exacerbation of AD-like pathology, supporting the notion that chronic and prolonged activation of glia is detrimental in the context of neurodegenerative disease [81, 87, 134]. The gene discussed is S100B; the disease is neurodegenerative disease.