Lithium chloride increases the production of amyloid-beta peptide independently from its inhibition of glycogen synthase kinase 3.
作者： Christine Feyt , Pascal Kienlen-Campard , Karelle Leroy , Francisca N'Kuli , Pierre J. Courtoy
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摘要: Glycogen synthase kinase 3 (GSK3) is able to phosphorylate tau at many sites that are found be phosphorylated in paired helical filaments Alzheimer disease. Lithium chloride (LiCl) efficiently inhibits GSK3 and was recently reported also decrease the production of amyloid-beta peptide (Abeta) from its precursor, amyloid precursor protein. Therefore, lithium has been proposed as a combined therapeutic agent, inhibiting both hyperphosphorylation Abeta. Here, we demonstrate inhibition by LiCl induced nuclear translocation beta-catenin Chinese hamster ovary cells rat cultured neurons, which phosphorylation observed. In cellular models, nontoxic concentration increased Abeta increasing beta-cleavage protein, generating more substrate for an unmodified gamma-secretase activity. SB415286, another inhibitor, slightly decreased production. It concluded LiCl-mediated increase not related inhibition.
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