Publication | Open Access
miR-15b represses BACE1 expression in sporadic Alzheimer’s disease
56
Citations
8
References
2017
Year
Neurochemical BiomarkersSynaptic SignalingSocial SciencesNeuroinflammationAlzheimer's DiseaseSporadic Alzheimer ’NeurologyBrain PathologyNeurogeneticsMolecular NeuroscienceBrain-immune InteractionAlzheimer DiseaseNeurodegenerationGene ExpressionMicrorna DetectionCell BiologyProtective MechanismsNeurodegenerative DiseasesBiomarkersSporadic AdNeuroscienceMedicine
Beta-site Amyloid precursor protein Cleaving Enzyme 1 (BACE1) is conceived as a potential target for therapies against Alzheimer disease (AD). MicroRNAs (miRNAs) are small non-coding RNAs that negatively regulate gene expression in a sequence-specific manner. Although miRNAs have been increasingly recognized as important modulators in sporadic AD. In order to confirm whether miR-15b correlates with the BACE1 upregulation in sporadic AD, we firstly evaluated the expression of miR-15b and BACE1 in sporadic AD brain tissues and analyzed the correlation of miR-15b with BACE1. Then we determined the regulation of miR-15b in SH-SY5Y cells on the BACE1 expression. And finally we determined the targeting to 3' UTR of BACE1 by miR-15b by a luciferase reporter. Downregulation of miR-15b alleviated Aβ-induced viability inhibition and decreased apoptosis in SH-SY5Y cells. Our results demonstrated that miR-15b play an important role in the cellular AD phenotype and might be involved in the pathogenesis of AD.
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