In vivo imaging of microglial activation with [11C](R)-PK11195 PET in idiopathic Parkinson's disease

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

  • Alexander Gerhard, Imperial College London, London, UK., Hammersmith Hospital
  • ,
  • Nicola Pavese
  • Gary Hotton, Imperial College London, London, UK.
  • ,
  • Federico Turkheimer, Imperial College London, London, UK.
  • ,
  • Meltem Es, Imperial College London, London, UK.
  • ,
  • Alexander Hammers, Imperial College London, London, UK., MRC Prion Unit, Institute of Neurology
  • ,
  • Karla Eggert, Philipps-Universität Marburg
  • ,
  • Wolfgang Oertel, Philipps-Universität Marburg
  • ,
  • Richard B. Banati, Imperial College London, London, UK., Sydney University, Sydney
  • ,
  • David J. Brooks

Idiopathic Parkinson's disease (PD) is a neurodegenerative disorder associated with akinesia, tremor and rigidity. While the characteristic Lewy body pathology targets pigmented and other brainstem nuclei at post-mortem, activated microglia are found in both subcortical and cortical areas. [ 11C](R)-PK11195 is a positron emission tomography (PET) marker of peripheral benzodiazepine sites (PBBS), which are selectively expressed by activated microglia. We examined 18 PD patients clinically and with [ 11C](R)-PK11195 and [18F]-dopa PET. Compared to 11 normal controls, the PD patients showed significantly increased mean levels of [ 11C](R)-PK11195 binding in the pons, basal ganglia and frontal and temporal cortical regions. Eight PD patients were examined longitudinally, and their [11C](R)-PK11195 signal remained stable over 2 years. Levels of microglial activation did not correlate with clinical severity or putamen [18F]-dopa uptake. Our in vivo findings confirm that widespread microglial activation is associated with the pathological process in PD. The absence of significant longitudinal changes suggests that microglia are activated early in the disease process, and levels then remain relatively static, possibly driving the disease via cytokine release.

Original languageEnglish
JournalNeurobiology of Disease
Pages (from-to)404-412
Number of pages9
Publication statusPublished - 1 Feb 2006
Externally publishedYes

    Research areas

  • Microglia, Neuroinflammation, Parkinson's disease, PET, PK11195

See relations at Aarhus University Citationformats

ID: 131161125