2026-06-14T03:29:38Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/75702024-10-31T11:40:31Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605
Repisalud
author
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
funder
Ministerio de Ciencia e Innovación (España)
funder
Ministerio de Educación y Ciencia (España)
funder
Fundación Ramón Areces
2019-05-14T10:39:56Z
2019-05-14T10:39:56Z
2013
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
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.
eng
Increased learning and brain long-term potentiation in aged mice lacking DNA polymerase μ
journal article
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