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Trial Lecture – time and place
See Trial Lecture.
Adjudication committee
- First opponent: Managing Director, Professor Claus Normann, Universitätsklinikum Freiburg, Germany
- Second opponent: Professor Ian Kirk, University of Auckland, New Zealand
- Third member and chair of the evaluation committee: Associate Professor Ingrid Amalia Havnes, University of Oslo
Chair of the Defence
Professor Emeritus Leif Gjerstad, University of Oslo
Principal Supervisor
Senior Consultant and researcher Torbjørn Elvsåshagen, Oslo University Hospital and University of Oslo
Summary
Patients with schizophrenia or bipolar disorder show signs of reduced cortical synaptic plasticity.
Synaptic plasticity is the altered connection between neurons after stimulation. Synaptic plasticity in the human cortex can be produced non-invasively by exposing a person to intensive high-contrast visual stimulation, and measured with electroencephalography (EEG).
We have tested this technique for assessing synaptic plasticity, compared different analytic methods for extracting signal from the EEG, examined the extent to which this signal is altered in patients with schizophrenia or bipolar disorder, and the extent to which it is related to the genetics predisposing people to schizophrenia or bipolar disorder.
We found that changes in the EEG after visual stimulation, indicative of synaptic plasticty, lasted throughout the experiment (~55 minutes), and that a classical event-related components extraction approach to EEG analysis was sensitive to the most striking modulation effects.
In a case-control analysis, we found a reduction in these changes among patients with schizophrenia or bipolar disorder as compared to people free of psychiatric illness, indicating aberrant cortical synaptic plasticity in these disorders.
Aberrant synaptic plasticity can produce symptoms common in schizophrenia and bipolar disorders, such as hallucinations and avolition.
Finally, we found that polygenic risk for these disorders was associated with synaptic plasticity alterations, albeit in a paradoxical manner, synaptic plasticity alterations being lower with higher polygenic risk.
The results from this study substantiate the EEG approach to indexing synaptic plasticity in humans and inform current theories of schizophrenia and bipolar disorder pathophysiology.
Additional information
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