Journal
BRAIN RESEARCH BULLETIN
Volume 175, Issue -, Pages 254-262Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.brainresbull.2021.06.023
Keywords
MicroRNA-16-5p; B-cell translocation gene 2; Autophagy; Apoptosis; Alzheimer's disease
Categories
Funding
- Inner Mongolia Natural Science Foundation [2018MS08127]
- National Natural Science Foundation of China [81660720]
- Program for Young Talents of Science and Technology in Universities of Inner Mongolia Autonomous Region
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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.
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.
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