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Pathogenesis of miR-155 on nonmodifiable and modifiable risk factors in Alzheimer's disease

Jia-Jia Liu1,2, Yun-Fan Long3, Peng Xu4

  • 1Academy of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.

Alzheimer'S Research & Therapy
|July 14, 2023
PubMed

Insights

MicroRNAs (miRNAs) are key in Alzheimer's disease (AD) progression. MiR-155, a pro-inflammatory mediator, influences neuroinflammation and may offer novel diagnostic and therapeutic targets for AD.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Alzheimer's disease (AD) is a leading cause of dementia, characterized by cognitive and behavioral deficits.
  • The exact etiology of AD remains unclear, though age, genetics, and vascular factors are implicated.
  • MicroRNAs (miRNAs) are small non-coding RNAs regulating gene expression and show potential as disease biomarkers.

Purpose of the Study:

  • To review the role of miR-155 in Alzheimer's disease pathogenesis.
  • To explore the biological mechanisms underlying miR-155's effects in AD.
  • To highlight miR-155 as a potential target for AD diagnosis and treatment.

Main Methods:

  • Literature review focusing on miR-155 and Alzheimer's disease.
  • Analysis of studies investigating miRNA regulation in neuroinflammation.
  • Examination of miR-155's impact on beta-amyloid and tau pathology.

Main Results:

  • MiR-155 acts as a pro-inflammatory mediator in neuroinflammation.
  • MiR-155 is implicated in the progression of beta-amyloid and tau pathologies in AD.
  • MiRNAs are relatively stable in bodily fluids, supporting their use as biomarkers.

Conclusions:

  • MiR-155 plays a significant role in the inflammatory processes contributing to Alzheimer's disease.
  • Understanding miR-155's mechanisms offers potential for novel diagnostic and therapeutic strategies for AD.
  • Further research into miR-155 could lead to innovative approaches for managing Alzheimer's disease.
Keywords:
Alzheimer’s diseaseBiomarkerNeuroprotectionPathogenesismiR-155

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