Narrowing the Search for the Cause of Autism

Through a National Institute of Child Health and Human Development grant on the orbitofrontal-limbic dysfunction in autism, a consortium of researchers led by The University of Texas-Houston will study the neurobiology and neuropsychology of autism and continue to seek the answer to what causes the multi-faceted disorder in the brain.

"For this project, we propose that congenital or early environmental insults to this ventral neural network are at the origin of the core social symptoms of autism," explains Dr. Katherine A. Loveland, UT-Houston professor of psychiatry and behavioral sciences and principal investigator (PI) and program director of the $4.8 million grant. Dr. Jocelyne Bachevalier, a neurobiology and anatomy professor, is co-PI.

Through three research projects, testing will be done on the working hypothesis: early dysfunction of a neural network, including the orbitofrontal cortex and the amygdala, is at the origin of autism. Recent neurobiological and clinical studies have led to the hypothesis that two major subsystems feed into a common limbic system.

Research for the three projects and two core modules will be conducted by faculty from Baylor College of Medicine by Dr. Kathryn J. Kotrla and Dr. L. Anne Hayman; at Rice University by Dr. David M. Lane; at UT-Houston by Dr. Michael Brandt, Dr. Jack Fletcher, and Dr. Deborah A. Pearson; and at The University of Texas Medical Branch-Galveston by Dr. Bob Willcott. Many levels of examination will be done on children, ages 7-18 with and without autism, as well as rhesus monkeys.

The objective of the research is to help explain the major clinical features of autism, a lifelong developmental disorder, as well as the range of outcomes. Autism disrupts many essential functions including communication, social behavior, and play, but as a psychopathological process, it develops along with the child.

Drs. Loveland and Bachevalier, who have been collaborating on autism research for more than four years, have recently studied the relationship between the symptoms of autism and early dysfunction of the amygdala and other brain components. Dr. Bachevalier's research with primates has focused on the amygdala and the hippocampus and indicates the role they play in communication, social behavior and learning. "When there is damage to this part of the brain early in life, the monkey develops symptoms similar to those seen in an autistic human," observes Dr. Bachevalier.

Research on socio-emotional cognition and behavior in autism suggests that there is considerable behavioral and developmental heterogeneity even among those individuals who meet diagnostic criteria for autism. These findings raise the question, what is centrally "autistic" about these diverse individuals?

"The primary hypothesis of the research project is that developmental impairment of the orbitofrontal-limbic circuit of the brain, including the mesial-orbitofrontal cortex and amygdala, is a biological marker for autism," explains Dr. Loveland, an expert in the development of language and social behavior in autism, "and that the characteristic socio-emotional deficits of persons with autism are related to developmental impairment of this circuit."

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©2006 Texas Medical Center

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