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Iliya Lefterov1, Nicholas F Fitz1, Yi Lu1

  • 1Department of Environmental and Occupational Health, School of Public Health, University of Pittsburgh, Pittsburgh, PA, United States.

Frontiers in Neuroscience
|June 5, 2023
PubMed
Summary

The Apolipoprotein E4 (APOEε4) allele is the highest genetic risk for Alzheimer's disease (AD). This review explores genetic and epigenetic factors influencing APOE expression and its interaction with TREM2 in AD models.

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Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Apolipoprotein E4 (APOEε4) allele represents the highest genetic risk for Alzheimer's disease (AD).
  • Despite extensive research, the precise mechanisms by which APOEε4 confers AD risk remain unclear.
  • Current knowledge has not yielded effective preventative or therapeutic strategies for AD.

Purpose of the Study:

  • To review genetic and epigenetic regulatory mechanisms controlling APOE expression.
  • To investigate the interaction between APOE and TREM2 in the context of AD pathology.
  • To discuss the role of microglia and astrocytes in AD-like pathology using animal models.

Main Methods:

  • Review of existing literature on APOE and TREM2 genetics and epigenetics.
  • Analysis of animal models with targeted APOE replacement.
  • Focus on protein-protein interactions and glial cell roles in AD models.

Main Results:

  • APOEε4 inheritance significantly increases Alzheimer's disease risk.
  • Existing animal models do not fully replicate human APOE gene regulation.
  • Epigenetic regulation of APOE in response to insults is understudied.
  • APOE and TREM2 interactions are crucial in microglial and astrocyte functions in AD.

Conclusions:

  • Understanding APOE regulation and its interaction with other risk factors like TREM2 is critical for AD research.
  • Further investigation into epigenetic mechanisms and glial cell roles in animal models is warranted.
  • Developing targeted therapies requires a deeper understanding of APOE's complex role in AD pathogenesis.
Keywords:
APOEAlzheimer’s diseaseTREM2animal modelrisktranscriptional control

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