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Human apolipoprotein E allele-specific brain expressing transgenic mice

J D Smith1, J Sikes, J A Levin

  • 1Laboratory of Biochemical Genetics and Metabolism, The Rockefeller University, New York, NY 10021, USA. smithj@rockvax.rockefeller.edu

Neurobiology of Aging
|January 8, 1999
PubMed
Summary

Researchers developed transgenic mice expressing human apolipoprotein E (apoE) isoforms in the brain. These mice, lacking endogenous apoE, show robust human apoE expression and may help study Alzheimer

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Area of Science:

  • Neuroscience
  • Genetics
  • Biochemistry

Background:

  • Apolipoprotein E (apoE) plays a critical role in lipid transport and is implicated in neurodegenerative diseases.
  • The apoE4 isoform is a significant genetic risk factor for Alzheimer's disease (AD).
  • Understanding the specific functions of human apoE isoforms in the brain is crucial for elucidating AD pathogenesis.

Purpose of the Study:

  • To create and characterize transgenic mouse models expressing human apoE isoforms (E2, E3, E4) in the brain.
  • To investigate the expression patterns and distribution of human apoE in the absence of endogenous apoE.
  • To provide a tool for studying the mechanisms underlying apoE4's association with Alzheimer's disease.

Main Methods:

  • Generation of transgenic mice using human apoE gene fragments under the glial acidic fibrillary protein (GFAP) promoter.

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  • Assessment of transgene expression via RNase protection, immunohistochemistry, and Western blotting.
  • Breeding transgenic mice with apoE-deficient mice to eliminate endogenous apoE expression.

    • Main Results:

    • Robust expression of human apolipoprotein E (apoE) was confirmed in the brains of transgenic mice.
    • Human apoE was detected throughout the brain, co-localizing with glial acidic fibrillary protein.
    • Primary astrocyte cultures secreted human apoE into the medium.
    • Aged apoE4 transgenic mice did not exhibit senile plaques.

    Conclusions:

    • Transgenic mice expressing human apoE isoforms under the GFAP promoter successfully recapitulate brain apoE expression.
    • These mouse models lacking endogenous apoE are valuable tools for investigating the role of specific human apoE isoforms in neurological processes.
    • The absence of senile plaques in aged apoE4 mice warrants further investigation into the complex mechanisms of apoE4 in Alzheimer's disease.