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.
Trial Lecture – time and place
See Trial Lecture.
Adjudication committee
- First opponent: Associate Professor Nicholas Ashton, University of Gothenburg
- Second opponent: Senior Consultant/Neurologist Marc Suaréz-Calvet, Barcelona Beta Brain Research Center
- Third member and chair of the evaluation committee: Associate Professor Reidun Torp, University of Oslo
Chair of the Defence
Professor II Bjørnar Hassel, University of Oslo
Principal Supervisor
Senior Consultant Anne-Brita Knapskog, Oslo University Hospital
Summary
Dementia is the decline of cognitive functions such as memory to an extent that limits a person’s ability to perform daily tasks such as paying bills. The most common cause of dementia is Alzheimer’s disease, a progressive neurodegenerative disorder. However, Alzheimer’s disease begins in the brain several years before we see the first signs of dementia. By studying biomarkers of Alzheimer’s disease such as changes in the brain, the cerebrospinal fluid or blood, we hope to achieve earlier diagnosis, earlier intervention and eventually a cure. The aim of Mari Aksnes’ thesis was to test the use of small amyloidogenic aggregates, called nanoplaques, as biomarkers for Alzheimer’s disease. Aksnes and colleagues used a novel method, the Thioflavin-T Fluorescence Correlation Spectroscopy (ThT-FCS) assay, to measure nanoplaques in cerebrospinal fluid and blood serum of patients assessed at the Memory Clinic at Oslo University Hospital.
Nanoplaques were associated with levels of the protein amyloid-β in cerebrospinal fluid, a known marker of Alzheimer’s disease and with several cytokines, molecules that indicate inflammation in the brain. However, there was no relationship between nanoplaques and other known markers of Alzheimer’s disease, such as imaging of amyloid in the brain (amyloid-PET) or levels of tau in the cerebrospinal fluid. Nanoplaque levels in the cerebrospinal fluid were higher in patients with Alzheimer’s disease compared to other memory clinic patients, but including measurement of nanoplaques did not improve the identification of Alzheimer’s disease patients compared to already available biomarkers. Nanoplaque levels in serum did not differ between patients with Alzheimer’s disease and other memory clinic patients. Overall, based on these results it seems unlikely that nanoplaque levels could be used as a single biomarker to diagnose Alzheimer’s disease.
Additional information
Contact the research support staff.