miR-137 overexpression protects neurons from A?-induced neurotoxicity via ERK1/2

Accumulation of amyloid-? (A?) is implicated in the pathogenesis and development Alzheimer's disease (AD) it a prime suspect for causing neuronal loss cognitive deficits during AD. To explore mechanisms A?-induced neurodegeneration, we used A?-treated primary cortical neuron culture as cell model AD investigated function miR-137 this process. qRT-PCR western blot were to examine levels miR-137, AMPA receptors (AMPARs), p-ERK1/2, ERK1/2. MTT assay caspases 3 activity employed viability apoptosis. Dual-luciferase was validate interaction between We found that A? decreased viability, AMPAR levels, but increased caspase dose- time-dependent manner. Overexpression suppressed neurotoxicity. MiR-137 directly bound ERK1/2 mRNA negatively regulated its expression. Further, overexpression blocked effects mimics on These results provide strong evidence protects neurons against neurotoxicity via targeting