Pharmaceutical development for NDDs has traditionally targeted altered biochemical signaling pathways downstream of primary genetic alterations. However, an alternative, top-down, approach is to devise therapeutics that target the altered neural circuits that underlie the cognitive and behavioural symptoms. Such an approach is important for several reasons. For example, circuit def
icits may be amenable to late treatment even if critical periods are found for molecular and cellular based interventions.
Neural development represents a complex coordination of numerous molecular, cellular and circuit events. When these events are altered, either in their nature or developmental time-course, homeostatic mechanisms are recruited in an attempt to counteract the changes in the developmental program. This compensation for the primary causes of autism may result in a nervous system that is unaffected by correction of the primary genetic cause but remains malleable to circuit-based interventions.