PRKCE and Alzheimer disease: Our current finding–that bryostatin treatment dramatically reduced Aβ levels in monomeric Aβ-treated cells in vitro–agrees with our previous studies showing that in AD transgenic cell lines that overexpress Aβ genes, chronic administration of PKCε activators bryostatin, DCP-LA, or DHA-CP6 reduces Aβ secretion and Aβ accumulation, as well as increases ECE activation [18], [38].