Abstract
Amyloid-β1-42 (Aβ1-42 ) is strongly associated with Alzheimer's disease (AD). The aim of this study is to elucidate whether and how miR-6076 participates in the modulation of amyloid-β (Aβ)-induced neuronal damage. To construct the neuronal damage model, SH-SY5Y cells were treated with Aβ1-42 . By qRT-PCR, we found that miR-6076 is significantly upregulated in Aβ1-42 -treated SH-SY5Y cells. After miR-6076 inhibition, p-Tau and apoptosis levels were downregulated, and cell viability was increased. Through online bioinformatics analysis, we found that B-cell lymphoma 6 (BCL6) was a directly target of miR-6076 via dual-luciferase reporter assay. BCL6 overexpression mediated the decrease in elevated p-Tau levels and increased viability in SH-SY5Y cells following Aβ1-42 treatment. Our results suggest that down-regulation of miR-6076 could attenuate Aβ1-42 -induced neuronal damage by targeting BCL6, which provided a possible target to pursue for prevention and treatment of Aβ-induced neuronal damage in AD.