Fragile X mental retardation reversed in mice

With fragle X syndrome, the subject's mutation in a particular gene on the X chromosome leads to cognitive difficulties, all the way to mental retardation in the extreme. At the synaptic level, the dendrites seem to be thin, stubby and immature, impairing signal transmission.
A protein, actin, helps to shape dendrites (as well as other parts of the neuron). Actin, in turn, is regulated by the enzyme, p21-activated kinase (PAK). The researchers speculated that by knocking out PAK activity (genetically in this case), actin production would go up and make for healthier dendrites. Indeed, fragile X mice without PAK production showed more normal cognitive behavior.
So, theoretically, if PAK production could be inhibited in fragile X humans with a drug or something, things could look better for them. Who knows, however, about side effects.