CN regulates AΒ metabolism in astrocytes. (A) In resting astrocytes, BACE expression and activity levels are relatively low. (B) Activation of astrocytes with inflammatory mediators stimulates CN. Nuclear translocation of NFATs and possibly NFΚB leads to the transcriptional upregulation of the protease BACE1 (the rate limiting enzyme for production of neurotoxic AΒ peptides). Elevated levels of BACE1 are associated with the increased production of AΒ peptides, which further aggregate and form AΒ plaques.