Trial Lecture - time and place
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Adjudication committee
- 1st opponent: Senior Researcher Dr Michael Eriksen Benros, Københavns Universitetshospital
- 2nd opponent: Adjunct Professor Maj-Britt Rocio Posserud, Universitetet i Bergen
- Comittee Chair: Adjunct Professor Grete Dyb, University of Oslo
Chair of the Defence
Professor Emeritus Berit Grøholt
Principal Supervisor
Professor Ole A. Andreassen
Summary
In this thesis, Eva Hoseth aimed at increasing our knowledge of the immune mechanisms involved in severe mental disorders by investigating specific immune signaling pathways. She assessed differences between people with schizophrenia or bipolar disorder and controls in plasma protein levels and gene expression, as well as potential connections to memory, brain MRI volumes and psychotropic medication.
The tumor necrosis factor pathway, or so called TNF pathway, and the Notch signaling pathway are two immune system related pathways. Hoseth showed that patients with severe mental disorders have increased TNF pathway activity and possible attenuated Notch signaling.
Increased TNF pathway activity was associated with lower performance on memory tests, while no significant associations were established with severity of clinical symptoms. Lithium, a medication for bipolar disorder, was associated with elements of both the TNF and Notch signaling pathways.
Circulating leukocytes and cells of the dorsolateral prefrontal cortex are an unlikely source for the increased TNF pathway activity. The source of the pro-inflammatory imbalance remains elusive and future studies are needed to explore the immune system.
Overall, the results further implicate the immune system in severe mental disorders and suggest some specific mechanisms that may be involved. Hoseth’s findings support an imbalance in the immune system in severe mental disorders, where increased immune activity is associated with impaired memory performance. Immune pathways could be relevant in the treatment of severe mental disorders as well as in managing lithium side effects.
Additional information
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