Abstract
Background/Aims: Leptin, an adipocytokine produced endogenously in the brain, is decreased in Alzheimer's disease(AD) and has also been shown to reduce Aβ levels in vitro and in vivo. Sets of evidence show that leptin reduces Aβ production and tau phosphorylation in neuronal cells and transgenic mice models of AD. Herein, we investigated the signaling pathway activated by leptin, to better understand its mechanism of action. Methods: Western blotting was performed to assess the levels of phosphor-tau and Bax, RT-PCR to check the mRNA level of Bax. Results: Leptin treatment significantly blunted Aβ-evoked tau phosphorylation and Bax levels, effects of which could be reversed by antagonist of Wnt signaling. Conclusion: The data indicate that Leptin may provide a novel therapeutic approach to AD treatment via wnt signaling.
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