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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
PubMed

Insights

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.
Keywords:
Alzheimer’s diseaseBACE2Let-7cRNA activationβ-amyloid

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