A sluggish DNA-repair system in mice is sufficient to reproduce the pathology and symptoms typical of neurodegenerative diseases.

Ype Elgersma and Dick Jaarsma at the Erasmus University Medical Center in Rotterdam, the Netherlands, and their colleagues deleted a gene in mice that is crucial to three DNA-repair mechanisms. Young adult mice developed learning and memory problems, and their neurons were less able to form strong connections with one another than were those of non-mutated mice of the same age. The mutant brains also showed signs of cell death and neurodegeneration.

The authors say that the accumulation of DNA damage may contribute directly to cognitive decline and pathology in conditions such as Alzheimer's disease.

J. Neurosci. 31, 12543–12553 (2011)