Public defence: Nathalia Zak
Cand.med. Nathalia Zak at Institute of Clinical Medicine will be defending the thesis “A longitudinal investigation of cortical plasticity and structure in bipolar disorder type II” for the degree of PhD (Philosophiae Doctor).
Trial Lecture – time and place
See Trial Lecture.
- First opponent: Managing Medical Director Claus Normann, Klinik Für Psychiatrie und Psychotherapie
- Second opponent: Professor Åsa Hammar, University of Bergen
- Third member and chair of the evaluation committee: Professor Svend Davanger, University of Oslo
Chair of the Defence
Professor Stein E. Opjordsmoen Ilner, University of Oslo
Post.doc. Torbjørn Elvsåshagen, University of Oslo
Bipolar disorder type II is characterized by episodes of hypomania and depression, and can cause substantial social and occupational impairments. Increased insight into pathophysiological mechanisms is essential for development of more effective therapeutic strategies and improvement of patient outcomes.
Bipolar disorders have recently been conceptualized as genetically influenced disorders of synaptic function and plasticity. Furthermore, loss of dysfunctional synapses in bipolar disorders might disrupt neural circuitry involved in mood and emotion regulation. Previous cross-sectional studies found impaired visual evoked potential plasticity, i.e., a likely in vivo correlate of cortical synaptic plasticity, and reduced thickness in frontal and temporal cortices in individuals with bipolar disorder type II compared to healthy control subjects. Whether these changes represent stable traits predisposing to illness or effects of mood episodes remains to be clarified.
The aim of this thesis was to contribute to greater understanding of cortical alterations and their longitudinal trajectories in bipolar disorder type II. To this end, adults with bipolar disorder type II and healthy controls underwent examinations of visual evoked potential plasticity and magnetic resonance imaging at baseline, and on average 2.4 years later. The findings indicate that impaired cortical plasticity and reduced frontotemporal cortical thickness might be stable traits in adults with bipolar disorders type II, and that mood episodes might cause further deterioration of these abnormalities. Finally, the results point to an association between cortical plasticity and longitudinal changes in cortical thickness.
These results advance the understanding of neurobiological changes associated with bipolar disorder type II, and support recent disease models, which suggest that impaired synaptic function and plasticity in frontotemporal brain regions might contribute to disrupted mood regulation.
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