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Silencing of lncRNA PRR34-AS1 Alleviates Alzheimer's Disease by Targeting miR-29c-3p to Regulate Microglia

Xing Cheng1, Hong-Fang Chen1, Jian-Wei Wang1

  • 1Department of Neurology, The Affiliated Jinhua Hospital, Zhejiang University School of Medicine, Jinhua, China.

Psychogeriatrics : the Official Journal of the Japanese Psychogeriatric Society
|May 12, 2025
PubMed
Abstract

Insights

Long non-coding RNA PRR34-AS1 is elevated in Alzheimer's disease (AD) patients, while miR-29c-3p is decreased. Inhibiting PRR34-AS1 reduces neuroinflammation and apoptosis in AD models, with miR-29c-3p mediating this effect.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Alzheimer's disease (AD) is a progressive neurodegenerative disorder.
  • Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) are implicated in AD pathogenesis.
  • The lncRNA PRR34 antisense RNA 1 (PRR34-AS1) and microRNA miR-29c-3p roles in AD require further elucidation.

Purpose of the Study:

  • To investigate the expression and mechanism of lncRNA PRR34-AS1 and miR-29c-3p in Alzheimer's disease.
  • To explore the regulatory axis between PRR34-AS1 and miR-29c-3p in AD.

Main Methods:

  • Serum samples from 35 AD patients and 35 healthy controls were analyzed.
  • In vitro studies used microglial cell lines (HMC3, BV2) treated with amyloid-beta (Aβ25-35).
  • RT-qPCR, dual luciferase reporter assays, RNA pull-down assays, CCK-8, and flow cytometry were employed.

Main Results:

  • PRR34-AS1 was upregulated, and miR-29c-3p was downregulated in AD patients' serum, showing a negative correlation.
  • Silencing PRR34-AS1 reduced Aβ25-35-induced microglial apoptosis and pro-inflammatory factor release.
  • A direct interaction between PRR34-AS1 and miR-29c-3p was confirmed; miR-29c-3p silencing reversed PRR34-AS1's anti-inflammatory effects.

Conclusions:

  • The PRR34-AS1/miR-29c-3p axis is critical in an Aβ25-35-induced AD cell model.
  • Inhibiting PRR34-AS1 alleviates neuroinflammation and apoptosis in microglial cells.
  • miR-29c-3p acts as a key mediator in the PRR34-AS1-driven AD pathway.
Keywords:
ADPRR34‐AS1inflammationmiR‐29c‐3pmicroglia

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