Due to copyright issues, an electronic copy of the thesis must be ordered from the faculty. For the faculty to have time to process the order, the order must be received by the faculty at the latest 2 days before the public defence. Orders received later than 2 days before the defence will not be processed. After the public defence, please address any inquiries regarding the thesis to the candidate.
Trial Lecture – time and place
See Trial Lecture.
- First opponent: Professor Sir Robin Murray, King's College London, UK
- Second opponent: Associate Professor Catharina Lavebratt, Karolinska Institutet, Sweden
- Third member and chair of the evaluation committee: Associate Professor Suraj Thapa, University of Oslo
Chair of the Defence
Professor II Jan Ivar Røssberg, University of Oslo
Associate Professor Nils Eiel Steen, University of Oslo
Schizophrenia and bipolar spectrum disorders are severe mental disorders with overlapping clinical features and risk factors. The exact underlying biological mechanisms are not clear; however, both disorders have high estimated heritability and genetic signals from immune loci, associations with previous infections and autoimmune comorbidity indicate a link with the immune system, further supported by repeated findings of abnormal levels of peripheral immune markers in these disorders. Standard pharmacological treatment is ineffective for about one third of patients, causing a significant burden.
In the current thesis we investigated whether genetic susceptibilities identified for autoimmune diseases, mental disorders, cognition and personality traits, number of previous infections and presence of autoimmune disease could explain immune marker aberrations in patients with severe mental disorders. Additionally, we investigated whether genetic susceptibility to schizophrenia is related to treatment resistance to antipsychotics.
Participants were included from the ongoing Thematically Organized Psychosis study, and well-adjusted analysis of covariance and logistic regression were applied to test associations.
There were few associations, except for between autoimmune disease, genetic susceptibility to schizophrenia and genetics associated with educational attainment and some of the immune markers. Moreover, we found an association between higher genetic susceptibility to schizophrenia and treatment resistance to antipsychotics. Our findings indicate a small role for autoimmune mechanisms and genetic susceptibilities to schizophrenia and educational attainment in low-grade inflammation in severe mental disorders, and for genetic susceptibility to schizophrenia in treatment resistance to antipsychotics. The very little explained variance and few associations suggest that immune marker abnormalities in these disorders are mainly explained by other factors.
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