Hippocampal adult neurogenesis is maintained by Neil3-dependent repair of oxidative DNA lesions in neural progenitor cells
Sunday, Oct 14, 2012, 10:00 AM -11:00 AM
C. E. REGNELL
, G. A. HILDRESTRAND
, Y. SEJERSTED
, T. MEDIN
, O. MOLDESTAD
, V. ROLSETH
, S. Z. KROKEIDE
, R. SUGANTHAN
, L. LUNA
, *J. STORM-MATHISEN
, M. BJORAS
, L. H. BERGERSEN
Univ. Oslo, Oslo, Norway;
Univ. Copenhagen, Copenhagen, Denmark
Accumulation of oxidative DNA damage has been proposed as a potential cause of age- related cognitive decline. The major pathway for removal of oxidative DNA base lesions is base excision repair, which is initiated by DNA glycosylases. In mice, Neil3 is the main DNA glycosylase for repair of hydantoin lesions in single stranded DNA of neural stem/progenitor cells, promoting neurogenesis. Adult neurogenesis is crucial for maintenance of hippocampus-dependent functions involved in behavior. Herein, behavioral studies revealed learning and memory deficits and reduced anxiety-like behavior in
mice. Neural stem/progenitor cells from aged
mice showed impaired proliferative capacity. Further, hippocampal neurons in
mice displayed synaptic irregularities. It appears that Neil3-dependent repair of oxidative DNA damage in neural stem/progenitor cells is required for maintenance of adult neurogenesis to counteract the age associated deterioration of cognitive performance.
The Norwegian Health Association
The Norwegian Cancer Society
The Research Council of Norway
[Authors]. [Abstract Title]. Program No. XXX.XX. 2012 Neuroscience Meeting Planner. New Orleans, LA: Society for Neuroscience, 2012. Online.
2012 Copyright by the Society for Neuroscience all rights reserved. Permission to republish any abstract or part of any abstract in any form must be obtained in writing by SfN office prior to publication.
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