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Inhibition of miR-4763-3p expression activates the PI3K/mTOR/Bcl2 autophagy signaling pathway to ameliorate cognitive

Wenxin Qi1,2, Yiwei Ying1,2, Peiru Wu1

  • 1School of Life Sciences, Shanghai University, Shanghai, China.

International Journal of Biological Sciences
|December 12, 2024
PubMed

Insights

MicroRNA miR-4763-3p is upregulated in Alzheimer's disease mild cognitive impairment (AD-MCI). Inhibiting this microRNA in mice improved cognitive function by reducing neuroinflammation and neuronal apoptosis.

Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Alzheimer's disease (AD) involves cognitive decline, memory impairment, neuronal apoptosis, and synaptic damage.
  • Aberrant microRNA regulation is implicated in AD pathogenesis, particularly in early stages like mild cognitive impairment (AD-MCI).

Purpose of the Study:

  • To identify the role of miR-4763-3p in AD pathogenesis, specifically in AD-MCI.
  • To investigate miR-4763-3p as a potential therapeutic target for AD-MCI.

Main Methods:

  • Fluorescence in situ hybridization to detect miR-4763-3p in AD hippocampal tissue.
  • Antagomir-mediated inhibition of miR-4763-3p in AD-MCI mouse models.
  • RNA-sequencing and functional assays to identify miR-4763-3p targets and pathways.

Main Results:

  • miR-4763-3p was upregulated in AD hippocampal tissue, colocalizing with Aβ and Tau.
  • Inhibition of miR-4763-3p ameliorated cognitive decline in AD-MCI mice.
  • miR-4763-3p targets ATP11A, promotes neuronal apoptosis, and modulates the PI3K/AKT/mTOR/Bcl2 pathway.

Conclusions:

  • miR-4763-3p plays a critical role in AD-MCI pathogenesis.
  • Inhibiting miR-4763-3p enhances neuronal autophagy, facilitates Aβ/lipofuscin clearance, reduces neuroinflammation and apoptosis, and improves cognitive function.
  • miR-4763-3p represents a promising therapeutic target for AD-MCI.
Keywords:
AD-MCIapoptosisautophagyphosphatidylserine

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