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Título: | Increased Learning and Brain Long-Term Potentiation in Aged Mice Lacking DNA Polymerase μ |
Autor: | Lucas, Daniel; Delgado-García, José María CSIC; Escudero, Beatriz CSIC; Albo, Carmen; Aza, Ana CSIC; Acín-Pérez, Rebeca; Torres, Yaima; Moreno, Paz; Enríquez, José Antonio; Samper, Enrique; Blanco Dávila, Luis; Fairén, Alfonso CSIC; Gruart, Agnès; Bernad, Antonio CSIC ORCID | Fecha de publicación: | 2013 | Editor: | Public Library of Science | Citación: | PLoS ONE 8 (2013) | Resumen: | A definitive consequence of the aging process is the progressive deterioration of higher cognitive functions. Defects in DNA repair mechanisms mostly result in accelerated aging and reduced brain function. DNA polymerase ο is a novel accessory partner for the non-homologous end-joining DNA repair pathway for double-strand breaks, and its deficiency causes reduced DNA repair. Using associative learning and long-term potentiation experiments, we demonstrate that Polο-/- mice, however, maintain the ability to learn at ages when wild-type mice do not. Expression and biochemical analyses suggest that brain aging is delayed in Polο-/- mice, being associated with a reduced error-prone DNA oxidative repair activity and a more efficient mitochondrial function. This is the first example in which the genetic ablation of a DNA-repair function results in a substantially better maintenance of learning abilities, together with fewer signs of brain aging, in old mice. © 2013 Lucas et al. | URI: | http://hdl.handle.net/10261/97736 | DOI: | 10.1371/journal.pone.0053243 | Identificadores: | doi: 10.1371/journal.pone.0053243 issn: 1932-6203 |
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