Por favor, use este identificador para citar o enlazar este Item:http://hdl.handle.net/20.500.12105/7570
Título
Increased learning and brain long-term potentiation in aged mice lacking DNA polymerase μ
Autor(es)
Lucas, Daniel | Delgado-García, José M | Escudero, Beatriz CNIC | Albo-Castellanos, Carmen CNIC | Aza, Ana CNIC | Acin-Perez, Rebeca CNIC | Torres, Yaima CNIC | Moreno, Paz | Enriquez, Jose Antonio CNIC | Samper, Enrique CNIC | Blanco, Luis | Fairén, Alfonso | Bernad, Antonio CNIC | Gruart, Agnès
Fecha de publicación
2013
Cita
PLoS One. 2013; 8(1):e53243
Idioma
Inglés
Tipo de documento
journal article
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 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.
MESH
Animals | Behavior, Animal | Brain | Conditioning, Classical | DNA | DNA Repair | DNA-Directed DNA Polymerase | Hippocampus | Locomotion | Long-Term Potentiation | Male | Mice | Mice, Knockout | Oxidative Stress | Phenotype | Reproducibility of Results | Temperature | Aging | Learning
Versión en línea
DOI
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