Mari Aksnes

Doctoral Research Fellow - Department of Geriatric Medicine

Norwegian version of this page

Email mari.aksnes@medisin.uio.no

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Visiting address Kirkeveien 166 Bygg 20 0450 Oslo

Postal address Postboks 4956 Nydalen OUS HF Ullevål sykehus 0424 Oslo

Other affiliations Faculty of Medicine (Student)

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Research interests

I am interested in the biological changes associated with neurodegeneration; how does neurodegeneration develop in the brain and how does it affect brain function? Further understanding of these changes can hopefully contribute to better identification, treatment and prevention of neurodegenerative diseases like Alzheimer's disease.

In my PhD-project I am researching biomarkers for Alzheimer's disease, biological changes associated with the disease that can contribute to better and earlier diagnostics.

Background

Education

2018 -
University of Oslo, PhD fellow in Geriatrics and Neuroscience
2015-2017
Norwegian University of Science and Technology, MSc in Neuroscience
"Effect of cerebrospinal fluid from patients with Alzheimer's disease on protein expression in the hippocampal region of a transgenic rat model of Alzheimer's disease"
2012-2015
University of Durham, BSc in Psychology
"The effects of forced fixation on diagnostic and non-diagnostic facial features on emotion identification: Exploring the association with callous-unemotional traits, alexithymia and empathy"

Work experience

2018 - University of Oslo,
PhD fellow in Geriatrics and Neuroscience, Ullevål Dementia Research Group
2018 Oslo University Hospital, Maria Korsnes' research group
Research assistant
2017 - 2018 Forskerfabrikken
Course leader for two "Researcher"-courses for school children
2017 - Bjørknes Høyskole
Supervisor and examinator

Publications

Scientific articles and bookchapters

Aksnes, Mari; Aass, Hans Christian Dalsbotten; Tiiman, Ann; Edwin, Trine Holt; Terenius, Lars & Bogdanovic, Nenad [Show all 8 contributors for this article] (2021). Associations of cerebrospinal fluid amyloidogenic nanoplaques with cytokines in Alzheimer's disease. Translational Neurodegeneration. ISSN 2096-6466. 10(1). doi: 10.1186/s40035-021-00244-3. Full text in Research Archive
Aksnes, Mari; Tiiman, Ann; Edwin, Trine Holt; Terenius, Lars; Bogdanovic, Nenad & Vukojevic, Vladana [Show all 7 contributors for this article] (2021). Comparison of cerebrospinal fluid amyloidogenic nanoplaques with core biomarkers of Alzheimer's disease. Frontiers in Aging Neuroscience. ISSN 1663-4365. 12:608628, p. 1–11. doi: 10.3389/fnagi.2020.608628. Full text in Research Archive
Aksnes, Mari; Müller, Ebba Gløersen; Tiiman, Ann; Edwin, Trine Holt; Terenius, Lars & Rootwelt-Revheim, Mona-Elisabeth [Show all 9 contributors for this article] (2020). Amyloidogenic nanoplaques in cerebrospinal fluid: Relationship to amyloid brain uptake and clinical Alzheimer's disease in a memory clinic cohort. Journal of Alzheimer's Disease. ISSN 1387-2877. 77(2), p. 831–842. doi: 10.3233/JAD-200237. Full text in Research Archive Show summary
Background: Aggregation of amyloid-β (Aβ) is an early pathological event in Alzheimer’s disease (AD). Consequently, measures of pathogenic aggregated Aβ are attractive biomarkers for AD. Here, we use a recently developed Thioflavin-T-Fluorescence Correlation Spectroscopy (ThT-FCS) assay to quantify structured ThT-responsive protein aggregates, so-called nanoplaques, in the cerebrospinal fluid (CSF). Objective: The overall aim of this work was to assess whether ThT-FCS determined CSF nanoplaque levels could predict amyloid brain uptake as determined by 18F-Flutemetamol PET analysis. Further, we assess whether nanoplaque levels could predict clinical AD. Methods: Nanoplaque levels in the CSF from 54 memory clinic patients were compared between sub-groups classified by 18F-Flutemetamol PET as amyloid-positive or amyloid-negative, and by clinical assessment as AD or non-AD. Results: Nanoplaque levels did not differ between amyloid groups and could not predict brain amyloid uptake. However, nanoplaque levels were significantly increased in patients with clinical AD, and were significant predictors for AD when adjusting for age, sex, cognitive function, and apolipoprotein E (APOE) genotype. Conclusion: The concentration of nanoplaques in the CSF differentiates patients with clinical AD from non-AD patients.

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Published Jan. 14, 2019 11:51 AM - Last modified June 13, 2019 11:37 AM