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Aβ pathology downregulates brain mGluR5 density in a mouse model of Alzheimer

Minkyung Lee1, Hae-June Lee2, In Suh Park3

  • 1Department of Nuclear Medicine, School of Medicine, Inha University, Incheon, South Korea.

Neuropharmacology
|February 11, 2018
PubMed

Insights

This study found reduced metabotropic glutamate receptor 5 (mGluR5) expression in the brains of advanced Alzheimer's disease (AD) mouse models. Positron emission tomography and immunoassay confirmed lower mGluR5 levels, particularly in the limbic system.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Medical Imaging

Background:

  • Alzheimer's disease (AD) is a progressive neurodegenerative disorder.
  • Metabotropic glutamate receptor 5 (mGluR5) plays a role in synaptic plasticity and neuronal function.
  • Dysregulation of mGluR5 has been implicated in AD pathogenesis.

Purpose of the Study:

  • To investigate functional changes in mGluR5 expression in an advanced AD mouse model (5xFAD).
  • To quantify mGluR5 levels using positron emission tomography (PET) and immunoassay techniques.

Main Methods:

  • Utilized PET imaging with the mGluR5-specific radiotracer [18F]FPEB in 5xFAD and wild-type mice.
  • Quantified non-displaceable binding potential (BPND) using Logan's graphical analysis.
  • Validated PET findings through immunoblotting of brain tissue protein isolates.

Main Results:

  • PET imaging revealed significantly lower radioactivities in the hippocampus and striatum of 5xFAD mice compared to controls.
  • Estimated mGluR5 binding values were significantly reduced in 5xFAD mice.
  • Immunoblotting confirmed lower mGluR5 protein intensity in 5xFAD mice brain tissues.

Conclusions:

  • mGluR5 levels are significantly down-regulated in the limbic system of the 5xFAD mouse model of Alzheimer's disease.
  • These findings suggest a potential role for mGluR5 dysregulation in AD progression.
  • PET imaging with [18F]FPEB is a viable method for assessing mGluR5 changes in AD models.
Keywords:
5xFAD miceAlzheimer's diseasePET[(18)F]FPEBmGluR5β-Amyloid

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