Onset of psychosis is believed to be associated with neuronal dysregulation and degeneration. Reductions in brain volumes have been related in part to neuronal loss but more substantially to loss of neuronal connectivity, loss of dendritic spines, and reductions in supporting glial cells. These changes have been associated with alterations in neurotrophic factors in the brain. Recent evidence suggests that aggressive synaptic pruning may underlie onset of psychosis for some individuals (1). While reductions in regional brain volumes have been demonstrated in individuals in their first episode of schizophrenia, further deterioration has been shown to occur even after initiation of treatment (2, 3). The disruption of myelination has been proposed as one mechanism underlying these effects (4, 5). Duration of untreated psychosis is associated with both symptom severity and poor functional outcomes (6). Therefore, the time around onset of psychosis is considered a critical period when neuronal systems in the brain are vulnerable to deterioration, fragile, unstable, and in need of protection and, possibly, regeneration.