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Imaging Striatal Microglial Activation in Patients with Parkinson's Disease

Yuko Koshimori1, Ji-Hyun Ko2, Romina Mizrahi3

  • 1Division of Brain, Imaging and Behaviour-Systems Neuroscience, Toronto Western Research Institute, University Hospital Network, University of Toronto, Toronto, Ontario, Canada; Research Imaging Centre, Centre for Addiction and Mental Health, University of Toronto, Toronto, Ontario, Canada.

Plos One
|September 19, 2015
PubMed

Insights

This study explored [18F]-FEPPA, a translocator protein 18kDa (TSPO) radioligand, as a biomarker for neuroinflammation in Parkinson's disease (PD). Results showed genotype significantly impacted TSPO binding, but not disease status, suggesting complex interactions in PD neuroinflammation.

Area of Science:

  • Neuroimaging
  • Neuroinflammation
  • Parkinson's Disease Research

Background:

  • Neuroinflammation is a key factor in Parkinson's disease (PD) progression.
  • Translocator protein 18kDa (TSPO) is a biomarker for neuroinflammation.
  • [18F]-FEPPA is a second-generation TSPO radioligand for Positron Emission Tomography (PET).

Purpose of the Study:

  • To evaluate [18F]-FEPPA as a neuroinflammation biomarker in the striatum of Parkinson's disease patients.
  • To investigate the relationship between TSPO gene rs6791 polymorphism and striatal neuroinflammation in PD.
  • To quantify neuroinflammation using PET imaging in PD.

Main Methods:

  • Recruited participants based on TSPO rs6791 genotype: high-affinity binders (HABs), mixed-affinity binders (MABs), and low-affinity binders (LABs).
  • Administered [18F]-FEPPA PET scans to 16 PD patients and 16 healthy controls (HCs).
  • Calculated total distribution volume (VT) in the caudate nucleus and putamen using a two-tissue compartment model.

Main Results:

  • Genotype significantly affected [18F]-FEPPA VT in the caudate nucleus (p=0.001) and putamen (p<0.001).
  • No significant main effect of PD disease status or disease x genotype interaction was found on striatal VT.
  • In HABs, PD patients showed a 16% higher striatal VT than HCs; MABs showed -8% (caudate) and 3% (putamen) differences.

Conclusions:

  • [18F]-FEPPA PET did not reveal increased striatal TSPO expression in PD patients.
  • The rs6791 polymorphism significantly influences [18F]-FEPPA binding in the striatum.
  • Findings suggest complex interactions between TSPO genotype and neuroinflammation in Parkinson's disease.

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