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Transgenic mice expressing APP-C100 in the brain

R L Neve1, F M Boyce, D L McPhie

  • 1Department of Genetics, Harvard Medical School, Belmont, MA, USA.

Neurobiology of Aging
|March 1, 1996
PubMed
Summary

A fragment of the Alzheimer amyloid precursor protein (APP), called APP-C100, is toxic to nerve cells. Transgenic mice expressing APP-C100 exhibit Alzheimer's disease neuropathology, supporting its role in disease progression.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Alzheimer's disease (AD) is characterized by amyloid plaques and neurofibrillary tangles, but the interplay with neuronal degeneration is unclear.
  • A specific fragment of the amyloid precursor protein (APP), termed APP-C100, is hypothesized to be a key player in AD pathogenesis.
  • APP-C100, containing the A beta peptide, has demonstrated in vitro toxicity to neurons.

Purpose of the Study:

  • To investigate the role of the APP-C100 fragment in Alzheimer's disease neuropathology.
  • To develop and utilize transgenic mouse models to test the hypothesis that APP-C100 causes AD-like brain changes.
  • To establish animal models for studying the mechanisms of APP-C100-induced neuronal death.

Main Methods:

  • Development of transgenic mice expressing the APP-C100 fragment under the control of the dystrophin brain promoter.

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  • Delivery of the APP-C100 transgene to the mouse brain.
  • Analysis of neuropathological features in the brains of these transgenic animal models.

    • Main Results:

    • Transgenic mice expressing APP-C100 exhibited neuropathological features characteristic of Alzheimer's disease.
    • The developed animal models successfully replicated some key AD brain pathologies.
    • The in vitro toxicity of APP-C100 to nerve cells was confirmed and extended to an in vivo model.

    Conclusions:

    • The APP-C100 fragment plays a significant role in the neuropathology of Alzheimer's disease.
    • Transgenic mouse models expressing APP-C100 are valuable tools for studying AD mechanisms.
    • Further research using these models can elucidate the neuronal receptor interactions leading to C100-induced neurotoxicity.