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Microglial activation and amyloid deposition in mild cognitive impairment: a PET study

A Okello1, P Edison, H A Archer

  • 1Division of Neuroscience and Mental Health, Faculty of Medicine, Imperial College London, London, UK. aren.okello@imperial.ac.uk

Neurology
|January 6, 2009
PubMed
Abstract

Insights

In patients with mild cognitive impairment (MCI), amyloid deposition and microglial activation can be detected using PET scans. These pathologies may occur independently, suggesting anti-inflammatory therapies could be beneficial for Alzheimer's disease prevention.

Area of Science:

  • Neuroscience
  • Radiology
  • Pharmacology

Background:

  • Activated microglia are implicated in Alzheimer's disease (AD) pathogenesis, clustering around beta-amyloid (Abeta) plaques.
  • Microglial activation is a potential therapeutic target for AD and its prodrome, amnestic mild cognitive impairment (MCI).

Purpose of the Study:

  • To characterize in vivo the distribution of microglial activation and amyloid deposition in patients with amnestic MCI.
  • Utilize Positron Emission Tomography (PET) with (11)C-(R)-PK11195 and (11)C-PIB tracers.

Main Methods:

  • PET imaging with (11)C-(R)-PK11195 and (11)C-PIB was performed on 14 subjects with MCI.
  • Psychometric tests were administered to assess cognitive function.

Main Results:

  • 50% of MCI patients showed increased cortical (11)C-PIB retention (amyloid deposition).
  • 38% of MCI subjects exhibited increased (11)C-(R)-PK11195 uptake (microglial activation).
  • Increased amyloid deposition correlated with microglial activation in MCI, particularly in the frontal cortex, but these pathologies could occur independently.

Conclusions:

  • Amyloid deposition and microglial activation are detectable in vivo in approximately 50% of MCI patients.
  • These pathologies can manifest independently in MCI.
  • Detecting microglial activation in MCI suggests potential efficacy of anti-inflammatory therapies for AD prevention.

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