The University of Oslo arranges all public defences digitally this semester, thus the disputation will be held as a video conference over Zoom.
The public 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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Trial Lecture – time and place
Adjudication committee
- First opponent: Professor Charalampos Tzoulis, Haukeland University Hospital
- Second opponent: Professor Oskar Hansson, Lund University, Sweden
- Third member and chair of the evaluation committee: Associate Professor Mona Skjelland, University of Oslo
Chair of the Defence
Professor Hilde Loge Nilsen, University of Oslo
Principal Supervisor
Professor II Tormod Fladby, University of Oslo
Summary
Parkinson's disease is a neurodegenerative movement disorder with cognitive symptoms with similarities to Alzheimer´s disease. Mild cognitive impairment affects 15-20 % of patients in early stage. 80 % develop dementia within 20 years. There is a lack of knowledge about the mechanisms. Aggregation of misfolded and neurotoxic proteins such as a-synuclein, amyloid-β and tau leading to synaptic dysfunction and neurodegeneration in the cortex may be involved. No preventive treatment is available yet, but should be applied early in the pathological process to prevent dementia. The aim of this thesis was to explore potential early diagnostic biomarkers of cognitive impairment.
Early Parkinson´s disease patients and normal controls underwent cognitive testing. Lumbar puncture was performed to collect cerebrospinal fluid (CSF) and analyze the levels of a-synuclein, amyloid-β, tau and neurogranin, which are thought to reflect the pathological changes in the brain. MRI was conducted to measure sizes of hippocampal subfields and cortical thickness. FDG-PET was completed to measure cortical glucose metabolism reflecting synaptic activity.
The patients had lower levels of CSF a-synuclein, amyloid-β, tau and neurogranin compared to controls. Lower CSF amyloid-β level was associated with poorer memory and executive function. The patients had smaller hippocampal subfields, which were associated with poorer memory and visuospatial function, but not thinner cortical thickness compared to controls. There were correlations between cortical glucose hypometabolism and lower CSF a-synuclein, amyloid-β and neurogranin, which correlated with poorer memory and executive tests in the patients.
This suggests that lower levels of CSF amyloid-β, smaller hippocampal subfields and cortical glucose hypometabolism are potential early biomarkers, and that α-synuclein and amyloid-β dysmetabolism affect synaptic function leading to cognitive impairment in early Parkinson´s disease.
Additional information
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