Reversing the effects of fragile X syndrome.

This column focuses on recent research in which researchers at the Massachusetts Institute of Technology reversed several morphological, neurophysiological, and behavioral consequences of fragile X syndrome in a mouse model of this disorder. In so doing, this column brings together several issues raised in all three previous columns1Y3: the genetic basis of neuropsychiatric disease, the interaction of genes and the environment in developmental neuropsychiatric disorders, and how the molecular mechanisms underlying such disorders can point the way to effective therapies. Specifically, this issue’s column focuses on how synaptic plasticity, which underlies brain development as well as learning and memory, is abnormally regulated in fragile X syndrome and how this abnormality may be modulated by therapeutic interventions.