Neuroprotective effect of melatonin on soluble A beta(1-42)-induced cortical neurodegeneration via Reelin-Dab1 signaling pathway

摘要

Objective: Soluble A beta(1-42) oligomers play a vital role in the development and pathogenesis of Alzheimer's disease (AD). Melatonin could delay the progress of AD through multiple mechanisms. Reelin-Dab1 signaling plays an important role in AD, including neuronal function and synaptic plasticity. However, whether melatonin could exert its neuroprotective function against soluble A beta(1-42)-induced neurotoxicity during AD development through regulating Reelin-Dab1 signaling remains poorly understood.