This is exemplified by an ELF-EMF-induced elevation in the expression of IL-18BP, which provides a signal for terminating the IL-18 mediated inflammatory response, and a rise in TGF-β that can act as an anti-inflammatory cytokine and has shown neuroprotective effects under conditions relevant to AD and following CNS insult [31], [32]. This evidence concerns the gene TGFB1 and Alzheimer disease.