title: How far can mice carry autism research?
abstract: 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.
authors.affiliation: Broad Institute of MIT and Harvard, 75 Ames Street, Cambridge, MA 02142, USA. Electronic address: seh@harvard.edu.
authors.forename: Steven E
authors.initials: SE
authors.lastname: Hyman
mesh_terms: D000818:Animals; D001321:Autistic Disorder / Q000235:genetics* / Q000503:physiopathology*; D015816:Cell Adhesion Molecules, Neuronal / Q000235:genetics*; D006801:Humans; D008565:Membrane Proteins / Q000235:genetics*; D009419:Nerve Tissue Proteins / Q000235:genetics*
chemical_list: D015816:Cell Adhesion Molecules, Neuronal; D008565:Membrane Proteins; D009419:Nerve Tissue Proteins; C098004:neuroligin 3