2026-06-14T05:05:42Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/75702024-10-31T11:40:31Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605

00925njm 22002777a 4500 dc Lucas, Daniel author Delgado-García, José M author Escudero, Beatriz author Albo-Castellanos, Carmen author Aza, Ana author Acin-Perez, Rebeca author Torres, Yaima author Moreno, Paz author Enriquez, Jose Antonio author Samper, Enrique author Blanco, Luis author Fairén, Alfonso author Bernad, Antonio author Gruart, Agnès author 2013 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 µ 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 Polµ(-/-) 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 Polµ(-/-) 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. PLoS One. 2013; 8(1):e53243 10.1371/journal.pone.0053243 1932-6203 1932-6203 PloS one 23301049 http://hdl.handle.net/20.500.12105/7570 Increased learning and brain long-term potentiation in aged mice lacking DNA polymerase μ