Circ_0003611 regulates apoptosis and oxidative stress injury of Alzheimer's disease via miR-383-5p/KIF1B axis.

Alzheimer's disease (AD) is a high incidence neurodegenerative disease. Emerging evidence suggests that circular RNAs (circRNAs) play an important modulator in the pathogenesis of AD. The aim of this paper was to reconnoiter the effects of circular RNA_0003611 (circ_0003611) on Aβ-triggered neuronal injury in AD. In this work, the abundance of circ_0003611 was augmented in AD patients and SH-SY5Y and SK-N-SH cells treated with Aβ. Aβ-mediated cell proliferation, apoptosis, inflammatory response, oxidative stress, and glycolysis were abolished through circ_0003611 silencing. Circ_0003611 worked as a miR-383-5p sponge, and the protective role of circ_0003611 absence on Aβ-triggered neuronal injury was overturned by releasing miR-383-5p. Meanwhile, miR-383-5p directly targeted KIF1B, and miR-383-5p upregulation might relieve Aβ-triggered neuronal injury by reducing KIF1B expression. Mechanical analysis discovered that circ_0003611 served as a sponge of miR-383-5p to impact KIF1B expression. These findings indicated that circ_0003611 improved Aβ-triggered neuronal injury in AD through targeting the miR-383-5p/KIF1B axis, which might deliver innovative therapy targeting for AD.