The public defence will be held as a video conference over Zoom.
The defence will follow regular procedure as far as possible, hence it will be open to the public and the audience can ask ex auditorio questions when invited to do so.
Click here to participate in the public defence
Due to copyright reasons, an electronic copy of the thesis must be ordered from the faculty. In order for the faculty to have time to process the order, it must be received by the faculty no later than 2 days prior to the public defence. Orders received later than 2 days before the defence will not be processed. Inquiries regarding the thesis after the public defence must be addressed to the candidate.
Digital Trial Lecture – time and place
Adjudication committee
- First opponent: Associate Professor Mady Hornig, Columbia University Medical Center, USA
- Second opponent: Professor Maj-Britt Posserud, Haukeland University Hospital
- Third member and chair of the evaluation committee: Professor Emeritus Frode Vartdal, University of Oslo
Chair of the Defence
Professor Emeritus Ragnhild Emblem, University of Oslo
Principal Supervisor
Vice-rector for Research Heidi Ormstad, University of South-Eastern Norway
Summary
Autism spectrum disorder (ASD) constitutes a broad spectrum of heterogeneous neurodevelopmental disorders that all start at an early age. Although the pathogenesis of ASD is not completely understood, an altered immune response has been implicated. The overall aim of this research was to improve the understanding of abnormalities in the immune system, in the kynurenine pathway (KP) and neurotrophic factors and their possible interactions, in ASD and its diagnostic subgroups. To achieve this goal, we examined the serum/plasma levels of 12 different cytokines, tryptophan (TRP), tryptophan catabolites (TRYCATs), and brain-derived neurotrophic factor (BDNF), in 65 children with ASD and 30 healthy controls. In this study we found that the cytokine levels did not differ significantly between the ASD group overall and the healthy controls. However, a noticeably higher interleukin (IL)-8 and lower IL-10 levels were found in the childhood autism subgroup compared with controls. We found that the KA level was lower and the KYN/KA ratio was significantly higher in ASD children than in healthy controls, which might indicate that the level of neurotoxicity is higher and the kynurenine aminotransferase (KAT) activity is lower in ASD children. Finally, we found that the plasma level of BDNF was higher in children with ASD than in controls, and particularly high in ASD children with intellectual disability (ID; intelligence quotient <70). Our results demonstrate possible neuroinflammatory and neurotoxic activity in children with childhood autism and ID and may have important implications for future therapeutic strategies applied to children with autism.
Additional information
Contact the research support staff.