Affiliation: Department of Clinical Molecular Biology, University of OSlo and Akershus University Hospital
Contact: h.l.nilsen@medisin.uio.no
Research interest
Aging and mitochondrial dysfunction are two fundamental processes that contribute to neurodegenerative diseases. Although there is growing evidence that DNA repair sits at the intersection of these processes, the mechanisms are largely unknown. We have developed C. elegans models to study how DNA repair influences neuronal health over a natural life-course. The overarching goal of our research is to define the mechanisms by which DNA repair may drive neurodegeneration and how this is counteracted by in-born self-defense mechanisms. We combine a genetic approached supported by extensive phenotyping to identify the drivers of neurodegeneration on the cell, tissue, and organismal levels.
Short bio
I have an MSc in Biochemical engineering and PhD from Norwegian University of Science and Technology where I generated the first gene targeted knockout Ung-/- mouse model (Molecular Cell). During my post-doctoral training with the 2015 Nobel laureate in Chemistry Tomas Lindahl (London), I demonstrated that UNG2 is required for class switch recombination and to mount an effective antibody response (Current Biology).
I was the main author on the first paper reconstituting Base Excision Repair on nucleosomal substrates (EMBO J). As a Principal Investgator at the Biotechnology Centre at the University of Oslo, I demonstrated that RNA repair enzymes also contribute to RNA quality control (Molecular Cell, Cell Reports) and established the first C. elegans laboratory in Norway. In C. elegans we study how DNA repair influences aging and neurodegeneration through cell autonomous and cell non-autonomous mechanisms (Cell, Cell Metabolism, Nature Neuroscience, PNAS, Nature Communications, Nucleic Acids Research, EMBO reports).
Publications:
- See list of publications at Nilsen's webpages at the University of Oslo
- See list of publications at Google Scholar
- See list of publications at ORCID
Supervisor for the following CompSci project
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Bioscience
- Modelling systems levels changes in brain aging induced by genome instability (available in call 1)