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| Toward a Neurogenetics of Problem Behavior |
| Monday, May 29, 2006 |
| 9:00 AM–10:20 AM |
| Baker |
| Area: CBM; Domain: Basic Research |
| Chair: Craig H. Kennedy (Vanderbilt University) |
| Discussant: Travis Thompson (University of Minnesota) |
| CE Instructor: Craig H. Kennedy, Ph.D. |
| Abstract: The causes of problem behavior involve environmental and biological determinants that impose organizational structure on responding. The past two decades have seen parallel, but separate innovations in (a) the functional analysis of problem behavior and (b) neurogenetics. The former innovations have allowed behavior analysts to identify and manipulate the discriminative stimuli, motivating operations, reinforcement contingencies, and reinforcing/punishing stimuli that influence response probability. The latter innovations have allowed for the molecular identification and measurement of single-nucleotide polymorphism (SNPs) occurring within genes that regulate neural circuitry function. In this symposium, we present data on the first synthesis of these two scientific domains. Our goal is to develop an integrated biobehavioral analysis of gene-brain-environment determinants of problem behavior. Each experiment will focus on problem behaviors, but within a distinct population. The experiments also build on each other by expanding the complexity of the SNPs and neural circuitry involved in the occurrence of problem behaviors. Our findings indicate distinct pattern of SNPs regulating monoaminergic circuits that are associated with the development and maintenance of behavior problems. |
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| Association between the Monoamine Oxidase A (MAOA) Gene and Chronic Problem Behavior in Adults with Developmental Disabilities. |
| MICHAEL E. MAY (Vanderbilt University), Laura Hodges (Vanderbilt University), John A. Phillips (Vanderbilt University), Randy D. Blakely (Vanderbilt University), Craig H. Kennedy (Vanderbilt University) |
| Abstract: A functional polymorphism in the promoter of the monoamine oxidase A (MAOA) gene has been associated with aggression in a general population sample of males. In this study, we sought to extend these findings to adults with developmental disabilities with histories of aggression. DNA samples and behavioral records were obtained from adult males with developmental disabilities, distinguished only by the presence or absence of aggression. These data were compared with a gender, ethnicity, and age-matched contrast sample. Our findings indicate that 54% of adults with developmental disabilities who were aggressive had the short allele version of the MAOA gene. In comparison, 23% of adults with developmental disabilities who were nonaggressive and 18% of the contrast group had the short allele MAOA polymorphism. Our findings suggest that a polymorphism in the MAOA gene may be associated with an aggressive phenotype in people with developmental disabilities. |
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| Associations among the MAOA and Serotonin Transporter (SERT) Genes and Problem Behavior in Children with Autism Spectrum Disorder. |
| JOHN A. W. JACKSON (Vanderbilt University), Michael E. May (Vanderbilt University), Christina F. Roantree (Vanderbilt University), Jill Parks (Vanderbilt University), Molly Ann McGinnis (Vanderbilt University), John A. Phillips (Vanderbilt University), Randy D. Blakely (Vanderbilt University), Craig H. Kennedy (Vanderbilt University) |
| Abstract: We analyzed SNPs in two genes – monoamine oxidase A (MAOA) and the serotonin transporter gene (SERT) – for an association with behavior problems in children with autism spectrum disorder (ASD). DNA samples and behavioral records were obtained from male children with ASD, along with behavioral samples using direct observation and interview. Our findings indicated a high correlation (.76) between the less efficient MAOA gene polymorphism and the degree of problem behaviors. There was a moderate association (.53) between autism severity, behavior problems, and MAOA gene polymorphism. No association was observed for type of ASD or polymorphisms in the SERT gene. Our findings suggest that polymorphisms in the MAOA gene are associated with problem behaviors in children with ASD and that a stronger association exists for those with a higher severity of autism. |
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| Associations among the MAOA, SERT, and catechol-O-methyl transferase Genes and Problem Behavior in Children with Severe Behavior Disorders. |
| CRAIG H. KENNEDY (Vanderbilt University), Joseph H. Wehby (Vanderbilt University), Christina F. Roantree (Vanderbilt University), Katherine Falk (Vanderbilt University), John A. Phillips (Vanderbilt University), Randy D. Blakely (Vanderbilt University) |
| Abstract: Problem behaviors affect a broad range of children and adolescents, from those with autism spectrum disorders to those with severe behavioral disorders (SBD). Although a range of treatments are being developed to reduce the occurrence of problem behavior, intervention is usually started after the onset of behavior problems. Yet to be established are neurobiological conditions that might increase the probability an individual develops behavior problems, thus potentially leading to prophylactic treatment. In this study, we analyzed three candidate genes for an association with problem behavior in children with SBD. We obtained participant characteristic and behavior problem data in the form of rating scales and direction observations from a group of males (age= 6 to 10 years) with SBD (N=60) and matched comparisons without SBD (N=60) and tested for associations with polymorphisms in the MAOA promoter gene, SERT gene, and catechol-O-methyl transferase (COMT) gene. We found positive associations between MAOA and COMT genes and problem behavior. In addition, there was a strong interaction between MAOA and COMT genes and the presence of environmental stressors, suggesting a gene x brain x environment effect on problem behavior. |
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