| First Author | Lucas D | Year | 2013 |
| Journal | PLoS One | Volume | 8 |
| Issue | 1 | Pages | e53243 |
| PubMed ID | 23301049 | Mgi Jnum | J:195819 |
| Mgi Id | MGI:5485325 | Doi | 10.1371/journal.pone.0053243 |
| Citation | Lucas D, et al. (2013) Increased learning and brain long-term potentiation in aged mice lacking DNA polymerase mu. PLoS One 8(1):e53243 |
| abstractText | 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 micro 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 Polmicro(-/-) 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 Polmicro(-/-) 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. |
