Journal
CELL
Volume 158, Issue 1, Pages 13-14Publisher
CELL PRESS
DOI: 10.1016/j.cell.2014.06.032
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In the face of growing controversy about the utility of genetic mouse models of human disease, Rothwell et al. report on a shared mechanism by which two different neuroligin-3 mutations, associated with autism spectrum disorders in humans, produce an enhancement in motor learning. The open question is how much we can learn about human ills from such models.
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