2024-03-28T20:01:15Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/977362021-12-28T16:37:47Zcom_10261_79com_10261_1com_10261_133col_10261_332col_10261_386
Increased Learning and Brain Long-Term Potentiation in Aged Mice Lacking DNA Polymerase μ
Lucas, Daniel
Delgado-García, José María
Escudero, Beatriz
Albo, Carmen
Aza, Ana
Acín-Pérez, Rebeca
Torres, Yaima
Moreno, Paz
Enríquez, José Antonio
Samper, Enrique
Blanco Dávila, Luis
Fairén, Alfonso
Gruart, Agnès
Bernad, Antonio
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.
2014-06-04T10:23:28Z
2014-06-04T10:23:28Z
2013
2014-06-04T10:23:28Z
artículo
PLoS ONE 8 (2013)
http://hdl.handle.net/10261/97736
10.1371/journal.pone.0053243
23301049
eng
Publisher’s version
openAccess
Public Library of Science