Previous research has suggested central nervous system inflammatory activity to be critically involved in disease development and progression in schizophrenia, with a complex interplay of inflammatory mechanisms leading to the development of brain abnormalities and medical symptoms related to schizophrenia. However, the mutual interactions of different inflammatory pathways and their relation to disease course have not been sufficiently studied. This study therefore aims to explore the interaction of neuroinflammatory mechanisms in patients with schizophrenia and to assess whether the inflammatory activity in schizophrenia is state-dependent and occurs mainly during psychotic episodes.
Name: [18F]-PBR111 Positron Emission Tomography (PET)
Name: Cognitive and psychomotor tasks
Name: Blood sampling
Description: Regional distribution volume in tissue (VT) of 2-(6-chloro-2-(4-(3-fluoropropoxy)phenyl)imidazo(1,2-a)pyridin-3-yl)-N,N-diethylacetamide (PBR111) labelled with fluorine-18 (18F) in schizophrenia patients and age- , gender-, and translocator protein (TSPO) binding profile- matched healthy controlsMeasure: Regional VT of [18F]PBR111 Time: 2 years
Description: Levels and ratios of inflammatory and neurotoxicity markers in blood samples of schizophrenia patients compared to healthy age- and gender-matched healthy controls.Measure: Peripheral markers Time: 2 years
There is one SNP
- Low affinity binder of the TSPO, as determined by rs6971 polymorphism genotyping at Screening - Use of benzodiazepines for 3x the half-life prior to PET-scan - Presence of irremovable magnetic materials in or on the body - Has a medical history of organic brain disease - Has a medical history of traumatic brain injury - Has a medical history of allergic reaction to any of the substances in the tracer fluid.