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dc.contributor.authorJalland, Clara Maria Osnes
dc.contributor.authorScheffler, Katja
dc.contributor.authorBenestad, Sylvie Lafond
dc.contributor.authorMoldal, Torfinn
dc.contributor.authorErsdal, Cecilie
dc.contributor.authorGunnes, Gjermund
dc.contributor.authorSuganthan, Rajikala
dc.contributor.authorBjørås, Magnar
dc.contributor.authorTranulis, Michael A.
dc.identifier.citationScientific Reports. 2016, 6.nb_NO
dc.description.abstractBase excision repair (BER) is the major pathway for repair of oxidative DNA damage. Mice with genetic knockout of the BER enzyme Neil3 display compromised neurogenesis in the sub-ventricular zone of the lateral ventricle and sub-granular layer of the dentate gyrus of the hippocampus. To elucidate the impact of oxidative DNA damage-induced neurogenesis on prion disease we applied the experimental prion disease model on Neil3-deficient mice. The incubation period for the disease was similar in both wild type and Neil3−/− mice and the overall neuropathology appeared unaffected by Neil3 function. However, disease in the Neil3−/− mice was of shorter clinical duration. We observed a mildly reduced astrogliosis in the hippocampus and striatum in the Neil3-deficient mice. Brain expression levels of neuronal progenitor markers, nestin (Nestin), sex determining region Box 2 (Sox2), Class III betatubulin (Tuj1) decreased towards end-stage prion disease whereas doublecortin (Dcx) levels were less affected. Neuronal nuclei (NeuN), a marker for mature neurons declined during prion disease and more pronounced in the Neil3−/− group. Microglial activation was prominent and appeared unaffected by loss of Neil3. Our data suggest that neurogenesis induced by Neil3 repair of oxidative DNA damage protects against prion disease during the clinical phase.nb_NO
dc.publisherNature Publishing Groupnb_NO
dc.rightsNavngivelse 4.0 Internasjonal*
dc.titleNeil3 induced neurogenesis protects against prion disease during the clinical phasenb_NO
dc.typeJournal articlenb_NO
dc.typePeer reviewednb_NO
dc.source.journalScientific Reportsnb_NO
dc.description.localcodeThis work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit
cristin.unitnameInstitutt for kreftforskning og molekylær medisin

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Navngivelse 4.0 Internasjonal
Except where otherwise noted, this item's license is described as Navngivelse 4.0 Internasjonal