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Neil3 induced neurogenesis protects against prion disease during the clinical phase
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Journal Article
Neil3 induced neurogenesis protects against prion disease during the clinical phase
2016
Overview
Base 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 beta-tubulin (
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.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 13/51
/ 38
/ 38/77
/ 64
/ 64/110
/ Animals
/ DNA
/ Gliosis
/ Humanities and Social Sciences
/ Lateral Ventricles - metabolism
/ Male
/ Mice
/ N-Glycosyl Hydrolases - genetics
/ N-Glycosyl Hydrolases - metabolism
/ Nestin
/ Science
/ Tubulin
