|Publication Type||Journal Article|
|Year of Publication||2014|
|Date Published||2014 Jul 03|
|Keywords||Animals, Autistic Disorder, Cell Adhesion Molecules, Neuronal, Humans, Membrane Proteins, Nerve Tissue Proteins|
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.