MicroRNA-146a regulates the expression of the Aβ1-42 protein in Alzheimer's disease

P Huang1, M Xu, Y-X He

  • 1Neurology, People's Hospital of Deyang City, Deyang, China. 1032857970@qq.com.

Abstract

Insights

MicroRNA-146a is differentially expressed in Alzheimer's disease (AD) patients and can predict AD. Its dysregulation may impact AD pathogenesis through signaling pathways.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Genetics

Background:

  • Alzheimer's disease (AD) is a progressive neurodegenerative disorder.
  • Biomarkers for early AD detection are crucial for effective management.
  • MicroRNAs (miRNAs) are implicated in various diseases, including neurodegeneration.

Purpose of the Study:

  • To investigate the expression and clinical significance of microRNA-146a, amyloid-beta 1-42 (Aβ1-42), and tau protein in peripheral blood of AD patients.
  • To evaluate the predictive value of microRNA-146a for AD.
  • To explore the potential mechanisms of microRNA-146a in AD pathogenesis.

Main Methods:

  • Peripheral blood samples were collected from 98 AD patients and 50 healthy controls.
  • Expression levels of microRNA-146a, Aβ1-42, and tau protein were measured.
  • Correlation analysis and receiver operating characteristic (ROC) curve analysis were performed.
  • Bioinformatics analysis was utilized to explore underlying mechanisms.

Main Results:

  • MicroRNA-146a, Aβ1-42, and tau protein showed differential expression in AD patients compared to controls (p<0.05).
  • MicroRNA-146a was negatively correlated with Aβ1-42 (r=-0.882, p<0.05).
  • ROC analysis indicated microRNA-146a has a predictive accuracy of 0.879 for AD.
  • Bioinformatics suggested microRNA-146a influences AD pathogenesis via Toll-like receptor and neurotransmitter signaling pathways.

Conclusions:

  • MicroRNA-146a, Aβ1-42, and tau protein are differentially expressed in the peripheral blood of AD patients.
  • MicroRNA-146a shows potential as a predictive biomarker for AD.
  • These molecules may contribute to AD pathogenesis by regulating signaling pathways and Aβ1-42 expression.

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