Background and activities
Neuroepigenetics - Base modifications in cognitive function
Genomic DNA is continuously challenged by endogenous and exogenous oxidative agents, thus preserving genomic integrity is a key for development and health. Base excision repair (BER) is the major pathway for removal of oxidized bases in the genome. BER is initiated by DNA glycosylases, recognizing and excising a broad range of base lesions. Several DNA glycosylases were identified as potential readers of epigenetic modifications and proteins involved in BER have been implicated in active DNA demethylation. Our recently published work revealed a function for DNA glycosylases beyond DNA repair in regulating gene expression related to adaptive behavior and cognition [Bjørge et al., Cell Reports, 2015] and in modulating the DNA methylome after myocardial infarction [Olsen et al., Cell Reports, 2017]
The main focus of my research is to unravel the molecular mechanism and function of DNA glycosylases in epigenetic remodeling in brain, thus laying the basis for novel therapeutic strategies for brain-related disorders such as Alzheimer’s disease.
- Nicole Bethge, PhD, Postdoc
- Milena Egiazarian, Forskerlinje student
- Silje Strømstad, Master student
- open position, Phd student
- open position, Postdoc
Education and Positions
- 2017 - present Principal Investigator, Department of Clinical and Molecular Medicine, Norwegian University of Science and Technology’s, Trondheim, Norway
- 2015 - 2017 Research Scientist, Department of Clinical and Molecular Medicine, Norwegian University of Science and Technology’s, Trondheim, Norway
- 2011 - 2014 Postdoc, Department of Medical Biochemistry, Oslo University and Oslo University Hospital, Norway
- 2007 - 2010 PhD, Neurodegeneration Research Laboratory, University of Rostock, Germany
- 2006 - 2007 Research assistant, Institute of Molecular Biology and Cancer Research, University of Marburg, Germany
- 2001- 2006 Diploma in Biochemistry, Institute of Medical Biochemistry and Molecular Biology, University of Greifswald, Germany
Olsen MB*, Hildrestrand GA*, Scheffler K*, Vinge LE, Alfsnes K, Palibrk V, Wang J, Neurauter CG, Luna L, Johansen J, Øgaard JD, Ohm IK, Slupphaug G, Kuśnierczyk A, Fiane AE, Brorson SH, Zhang L, Gullestad L, Louch WE, Iversen PO, Østlie I, Klungland A, Christensen G, Sjaastad I, Sætrom P, Yndestad A, Aukrust P, Bjørås M, Finsen AV (2017). NEIL3-Dependent Regulation of Cardiac Fibroblast Proliferation Prevents Myocardial Rupture. Cell Reports, 18(1):82-92.
Jalland CM, Scheffler K, Benestad SL, Moldal T, Ersdal C, Gunnes G, Suganthan R, Bjørås M, Tranulis MA (2016). Neil3 induced neurogenesis protects against prion disease during the clinical phase. Scientific Reports, 25;6:37844.
Bjørge MD*, Hildrestrand GA*, Scheffler K*, Suganthan R, Rolseth V, Kuśnierczyk A, Rowe AD, Vågbø CB, Vetlesen S, Eide L, Slupphaug G, Nakabeppu Y, Bredy TW, Klungland A, Bjørås M (2015). Synergistic Actions of Ogg1 and Mutyh DNA Glycosylases Modulate Anxiety-like Behavior in Mice. Cell Reports, 13(12):2671-8.
Strand JM*, Scheffler K*, Bjørås M, Eide L (2014). The distribution of DNA damage is defined by region-specific susceptibility to DNA damage formation rather than repair differences. DNA repair (Amst), 18:44-51.
Scheffler K, Krohn M, Dunkelmann T, Stenzel J, Hofrichter J, Lange C, Ibrahim S, Walker LC, Pahnke J, (2012) Mitochondrial DNA polymorphisms specifically modify cerebral β-amyloid proteostasis. Acta Neuropathologica, 124(2):199-208.
Krohn M, Lange C, Hofrichter J, Scheffler K, Stenzel J, Steffen J, Schumacher T, Brüning T, Plath AS, Alfen F, Schmidt A, Winter F, Rateitschak K, Wree A, Gsponer J, Walker LC, Pahnke J, (2011). Cerebral amyloid-b proteostasis is regulated by the membrane transport protein ABCC1 in mice. Journal of Clinical Investigation, 121(10):3924-3931.
* Authors contribute equally to the work