Bibliographic
Recent laboratory studies have demonstrated that administration of melatonin can attenuate Alzheimer-like tau hyperphosphorylation, Aβ overproduction, and behavioral deficits in cells and in rats . Because of the excellent bioavailability and lack of toxicity, melatonin could serve as an effective ameliorating reagent for AD.The goal of this study was to determine the efficacy of melatonin treatment on improving AD-like cognitive deficits and pathologies in the Tg2576 model at different stages of AD-like disease progression. this study the authors found that treatment of Tg2576 mice with melatonin from 4-8 months of age did not improve the pathology or behavioral performance of the mice. However, remarkable attenuation of tau and β-amyloid pathologies with memory improvement were observed when melatonin was supplied from the age of 8-12 months or 4-12 months of the mice. More importantly, the improvements were still significant when the mice survived to old age. In addition, the study found that the timely targeting of glycogen synthase kinase-3beta (GSK-3beta), the most implicated tau kinase, seems most critical for the efficacy of melatonin. The authors posit that melatonin treatment only at proper timing could arrest AD by targeting the activated GSK-3beta, which provides primary evidence for the importance and strategy in developing disease-modifying interventions of AD.