MicroRNA-16-5p/BTG2 axis affects neurological function, autophagy and apoptosis of hippocampal neurons in Alzheimer's disease

Objective: Studies have focused on the functions of microRNAs (miRNAs) in Alzheimer's disease (AD), but not much on miR-16-5p. Hence, this study intends to unearth the mechanism of AD, mainly focusing on miR-16-5p/ B-cell translocation gene 2 (BTG2) axis. Methods: APPswe/PS1dE9 mice were injected with depleted BTG2 and/or restored miR-16-5p vectors into the third ventricle to explore their roles in neurological function, neuronal damage, autophagy and apoptosis in AD mice. In vitro cultured hippocampal neurons were transfected with depleted BTG2 and/or restored miR-16-5p vector to interpret their functions in neuronal viability and apoptosis. MiR-16-5p and BTG2 expression in hippocampal tissues and neurons were detected. Results: Lower miR-16-5p and higher BTG2 expression levels were found in hippocampal tissues and neurons. MiR-16-5p up-regulation or BTG2 down-regulation improved neurological function and neuronal damage and inhibited neuronal autophagy and apoptosis in AD mice. Restored miR-16-5p or depleted BTG2 restrained neuronal viability and apoptosis in vitro. Conclusion: Our study reveals that restored miR-16-5p or depleted BTG2 protects neurological function and suppresses neuronal autophagy and apoptosis in AD mice, which renews a novel guide toward AD treatments from the perspective of miR-16-5p/BTG2 axis.

Automated summary

The study focused on the role of miR-16-5p and BTG2 in Alzheimer's disease, showing lower miR-16-5p and higher BTG2 expression levels in hippocampal tissues and neurons of AD mice. Restored miR-16-5p or depleted BTG2 protected neurological function and suppressed neuronal autophagy and apoptosis. This highlights a new potential therapeutic target in AD treatment through the miR-16-5p/BTG2 axis.