Trial Lecture – time and place
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Adjudication committee
- First opponent: Professor Robert Kumsta, Rühr-Universität Bochum, Germany
- Second opponent: Associate Professor Solveig Merete Klæbo Reitan, Norwegian University of Science and Technology (NTNU)
- Third member and chair of the evaluation committee: Associate Professor Ketil Hanssen-Bauer, Faculty of Medicine, University of Oslo
Chair of the Defence
Professor Emeritus Lars Weisæth, Faculty of Medicine, University of Oslo
Principal Supervisor
Professor Ole A Andreassen, Faculty of Medicine, University of Oslo
Summary
Schizophrenia is regarded as a complex disorder caused by genetic and environmental factors, but the underlying pathological mechanisms are still largely unknown. Dysregulation of antioxidant defense, impaired levels of antioxidants and lipid peroxidation have been suggested as possible pathophysiological mechanisms underlying schizophrenia development.
In a longitudinal study, patients with schizophrenia were examined in an acute phase and five year later in a stable phase. The aim of the study was to identify biological abnormalities and determine if these were dynamic and associated with clinical characteristics and disease phase.
Serum lipids were elevated both in the acute and the stable phase, while membrane lipid levels were low in the acute phase, but not in the stable phase. There was association between symptom intensity and lipid profiles in the stable phase, but not in the acute phase. Alpha-tocopherol levels were higher in the acute phase, and levels of antioxidants differed form healthy controls also in the stable phase.
The study indicates that oxidative dysregulation and lipid metabolism are involved in schizophrenia pathophysiology. The processes are dynamic and change during different phases of schizophrenia. Disease phase must be considered when studying lipids and antioxidants in schizophrenia. Lipid profiles, oxidative stress and antioxidants are potential biomarkers in schizophrenia.
Additional information
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