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Microglia, amyloid, and glucose metabolism in Parkinson's disease with and without dementia

Paul Edison1, Imtiaz Ahmed, Zhen Fan

  • 1Centre of Neuroscience, Department of Medicine, Imperial College London, London, UK.

Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology
|January 11, 2013
PubMed

Insights

Microglial activation, a marker of neuroinflammation, is elevated early in Parkinson's disease (PD) and Parkinson's disease dementia (PDD), independent of amyloid plaques. This neuroinflammation correlates with cognitive decline and reduced brain metabolism.

Area of Science:

  • Neuroimaging
  • Neurology
  • Molecular Imaging

Background:

  • Translocator protein upregulation signifies microglial activation, a key indicator in neurodegenerative diseases.
  • Amyloid deposition and cerebral glucose metabolism are also critical markers in Parkinson's disease (PD) spectrum disorders.
  • Investigating the interplay between neuroinflammation, amyloid pathology, and metabolic changes is crucial for understanding PD progression.

Purpose of the Study:

  • To assess in vivo the relationship between microglial activation, amyloid deposition, and glucose metabolism in Parkinson's disease dementia (PDD) and PD without dementia.
  • To determine if microglial activation is an early event in the PD spectrum and if it is independent of amyloid pathology.
  • To correlate neuroimaging findings with cognitive status.

Main Methods:

  • Positron Emission Tomography (PET) scans using [(11)C](R)PK11195 (microglial activation), [(11)C]PIB (amyloid), and [(18)F]FDG (glucose metabolism).
  • Magnetic Resonance Imaging (MRI) for anatomical reference.
  • Region of interest and statistical parametric mapping (SPM) analyses were performed on PET data.

Main Results:

  • PDD patients exhibited significant microglial activation in multiple cortical and subcortical regions compared to controls.
  • PD subjects without dementia showed increased microglial activation in temporal, parietal, and occipital regions.
  • Both PDD and PD groups displayed reduced cerebral glucose metabolism, while [(11)C]PIB uptake was only marginally increased. Microglial activation and reduced metabolism correlated with Mini-Mental State Examination scores.

Conclusions:

  • Cortical microglial activation and reduced cerebral glucose metabolism are detectable early in the Parkinson's disease spectrum.
  • Microglial activation may be a driving factor in Parkinson's disease dementia progression.
  • Therapeutic strategies targeting microglial activation could potentially influence disease progression.

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