Due to technical problems the defence has been moved from 11:15 to 11:45.
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.
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Digital Trial Lecture – time and place
Adjudication committee
- First opponent: Professor Joana de Almeida Santos Pacheco Palha, University of Minho, Portugal
- Second opponent: Associate Professor Cecília Reis Alves dos Santos, University of Beira Interior, Portugal
- Third member and chair of the evaluation committee: Researcher Tuula Anneli Nyman, University of Oslo
Chair of the Defence
Professor Trygve Brauns Leergaard, Faculty of Medicine, University of Oslo
Principal Supervisor
Professor Jens Pahnke, Faculty of Medicine, University of Oslo
Summary
With the global aging population, the graceful aging will become a goal. And dementia or loss of memory will be a major obstacle to attain this goal. Alzheimer’s disease (AD) is the most common cause of dementia. This PhD work has found avenues to contain AD dementia in AD disease mouse model.
Studies show that impairment in spatial memory is a harbinger of AD dementia. Spatial memory is generally understood as the memory of the external environment. In rodents, spatial memory is often measured using behavioral test such as Morris Water Maze (WM) task. Historically, the WM task was used to study the role of hippocampus in spatial learning and memory. Currently, it is the popular test of assessing spatial cognition in general.
This PhD thesis aimed at detecting spatial memory dysfunction in an AD mouse model at an early stage of disease pathogenesis. This dysfunction is referred to as mild cognitive impairment (MCI). Once the MCI was detected, the PhD thesis further aimed to protect the spatial memory via cognitive training or pharmacological manipulation.
In this APPPS1-21 AD mouse model, β-amyloid plaques–the hallmark of AD pathogenesis–appear in hippocampus from 3 months of age whereas cognitive dysfunction is reported at 7 months of age. Using the WM task, we detected mild cognitive impairment at the age of 3 months. Next, we studied the role of cognitive training on the fate of the spatial memory. We overtrained AD mice on a WM task at the age of 2 months, retrained them at 3 months, and finally assessed their cognition at 7 months of age. We found that cognitive dysfunction was contained in AD mice. Interestingly, the cognitive training acted as a double-edged role. On one hand, it contained cognitive dysfunction, but on the other hand it also decreased cognitive flexibility. Finally, we also showed that cognitive dysfunction was contained by the extract Pycnogenol.
In summary, this PhD thesis shows that cognitive dysfunction can be contained either by cognitive training or by pharmacological treatment. This thesis, therefore, lays ground for future investigations regarding brain mechanism for the relationship between containment of cognitive dysfunction and cognitive training.
Additional information
Contact the research support staff.