Increased learning and brain long-term potentiation in aged mice lacking DNA polymerase μ.

PloS one 2013

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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.

Citation

Daniel Lucas, José M Delgado-García, Beatriz Escudero, Carmen Albo, Ana Aza, Rebeca Acín-Pérez, Yaima Torres, Paz Moreno, José Antonio Enríquez, Enrique Samper, Luis Blanco, Alfonso Fairén, Antonio Bernad, Agnès Gruart. Increased learning and brain long-term potentiation in aged mice lacking DNA polymerase μ. PloS one. 2013;8(1):e53243