Abstract
Alzheimer's disease (AD) is the most common form of dementia; its pathophysiological mechanism remains unclear. Long noncoding RNAs (lncRNAs) play key roles in AD. lncRNA EBF3-AS has been found dysregulated in AD, which is abundantly expressed in the brain. The aim of this study was to investigate the role of EBF3-AS in AD. Results showed that the expressions of lncRNA EBF3-AS and EBF3 (early B cell factor 3) were upregulated in hippocampus of APP/PS1 mice (AD model mice). EBF3-AS knockdown by siRNA inhibited the apoptosis induced by Aβ25-35 and okadaic acid (OA) in SH-SY5Y. The expression of EBF3 was downregulated in Aβ25-35- and OA-treated SH-SY5Y, which was reversed by EBF3-AS knockdown. EBF3 knockdown can reverse the Aβ25-35-induced apoptosis in SH-SY5Y. These results revealed that lncRNA EBF3-AS promoted neuron apoptosis in AD, and involved in regulating EBF3 expression. EBF3-AS may be a new therapeutic target for treatment of AD.
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