APP and Alzheimer disease: Here, to investigate whether activated astrocytes could be significant sources of Aβ during AD neuroinflammation and whether an amyloidogenic astrocytic feed-forward mechanism may exist, we treated cultured primary wild-type C57BL/6J or Tg2576 mouse astrocytes with pro-inflammatory cytokine combinations or Aβ42 oligomers and fibrils and measured levels of BACE1, APP, secreted Aβ40, or APPsβsw, the β-secretase cleavage product.