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Let-7c increases BACE2 expression by RNAa and decreases Aβ production
Heng Liu1,2,3, Shuai Chen2,3, Qian Sun2,3
1School of Medicine, Cheeloo College of Medicine, Shandong University Jinan 250012, Shandong, China.
American Journal of Translational Research
|March 11, 2022
Summary
MicroRNA let-7c is elevated in Down syndrome and Alzheimer's disease, reducing amyloid-beta production by up-regulating BACE2 expression. This finding offers new insights into neurodegenerative disease mechanisms.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- MicroRNAs (miRNAs) are key gene regulators implicated in neurodegeneration.
- Alzheimer's disease (AD) and Down syndrome (DS) share pathological links.
- Understanding miRNA roles in AD pathogenesis is crucial.
Purpose of the Study:
- Investigate the role of miRNAs in AD pathogenesis using DS as a model.
- Determine the specific function of miRNA let-7c in relation to AD pathology.
Main Methods:
- TaqMan microRNA array for miRNA profiling.
- ELISA and RT-qPCR for quantifying let-7c and Aβ levels.
- Western blotting and luciferase reporter assays to elucidate molecular mechanisms involving BACE2.
Main Results:
- let-7c was significantly up-regulated in DS and AD models.
- let-7c reduced amyloid-beta (Aβ) levels.
- let-7c induced BACE2 expression, promoting C99 cleavage and decreasing Aβ production.
Conclusions:
- let-7c plays a protective role by down-regulating Aβ production.
- The study reveals a novel mechanism where let-7c up-regulates BACE2, offering a potential therapeutic target for AD.
