Neurochemical Developmental Regulation In Autism

Autistic behaviors are associated with multiple etiologies and may, therefore, result in heterogeneous responses to treatment. Regardless of etiology, however, it appears that autism is the consequence of deviations from normal brain developmental processes. Identification and delineation of the timing of these deviations from the normal developmental sequence may allow strategies for pharmacological intervention aimed at setting brain developmental programs back on course. Molecular imaging studies, using techniques such as positron emission tomography (PET), can provide information regarding time course differences in the ontogeny of various neurochemical processes in autism or subgroups of children with autism, and can therefore aid in designing treatment strategies with respect to timing of interventions. For example, studies using α[11C]methyl-L-tryptophan as a PET tracer to estimate serotonin synthesis showed that humans undergo a period of high brain serotonin synthesis capacity during childhood, and that this developmental process is disrupted in autistic children. Since serotonin is known to be an important factor involved in postnatal synaptogenesis, one approach to the treatment of autism would be the use of serotonergic agents in children less than the age of 6 years, when serotonin synthesis capacity is lower in autistic children compared to non-autistic controls. The goal of treatment would be to provide a more normal modulation of synaptic plasticity for a finite period of brain development. This talk will explore strategies for exploiting critical periods for therapeutic alteration of brain development in autism.