Published August 31, 2016 | Version v1
Journal article Open

In vivo (R)-[11C]PK11195 PET imaging of 18kDa translocator protein in recent onset psychosis

  • 1. Department of Psychiatry, Rudolf Magnus Institute for Neurosciences, University Medical Center Utrecht, Utrecht, The Netherlands and Department of Radiology & Nuclear Medicine, VU University Medical Center, Amsterdam, The Netherlands
  • 2. Department of Psychiatry, Rudolf Magnus Institute for Neurosciences, University Medical Center Utrecht, Utrecht, The Netherlands
  • 3. Department of Psychiatry, Academic Medical Center, Amsterdam, The Netherlands
  • 4. Department of Radiology & Nuclear Medicine, VU University Medical Center, Amsterdam, The Netherlands

Description

Evidence is accumulating that immune dysfunction is involved in the pathophysiology of schizophrenia. It has been hypothesized that microglia activation is present in patients with schizophrenia. Various in vivo and post-mortem studies have investigated this hypothesis, but as yet with inconclusive results. Microglia activation is associated with elevations in 18 kDa translocator protein (TSPO) levels, which can be measured with the positron emission tomography (PET) tracer (R)-[11C]PK11195. The purpose of the present study was to investigate microglia activation in psychosis in vivo at an early stage of the disease. (R)-[11C]PK11195 binding potential (BPND) was measured in 19 patients with recent onset psychosis and 17 age and gender-matched healthy controls. Total gray matter, as well as five gray matter regions of interest (frontal cortex, temporal cortex, parietal cortex, striatum, and thalamus) were defined a priori. PET data were analysed using a reference tissue approach and a supervised cluster analysis algorithm to identify the reference region. No significant difference in (R)-[11C]PK11195 BPND between patients and controls was found in total gray matter, nor one of the regions of interest. These findings suggest that microglia activation is not present in recent onset psychosis or that it is a subtle phenomenon that could not be detected using the design of the present study.

Files

Van der Doef_NPJSchizophr_2016-P09.pdf

Files (475.9 kB)

Name Size Download all
md5:0c590c132f46619a6cdbf617c9fecca3
475.9 kB Preview Download

Additional details

Funding

INMIND – Imaging of Neuroinflammation in Neurodegenerative Diseases 278850
European Commission