International Meeting for Autism Research (London, May 15-17, 2008): AGE-RELATED CHANGES IN CORPUS CALLOSUM MICROSTUCTURE

Saturday, May 17, 2008

Champagne Terrace/Bordeaux (Novotel London West)

11:30 AM

M. DuBray , Neuroscience and Psychiatry, University of Utah, Salt Lake City, UT

A. L. Alexander , Department of Medical Physics, Department of Psychiatry, Waisman Laboratory for Brain Imaging & Behavior, University of Wisconsin, Madison, WI

J. E. Lee , Medical Physics, University of Wisconsin, Madison, WI

M. Lazar , Center for Biomedical Imaging, New York University School of Medicine, New York, NY

A. Froehlich , Psychology, University of Utah, Salt Lake City, UT

N. Lange , Biostatistics, Laboratory for Statistical Neuroimaging McLean Hospital, Boston, MA

E. Bigler , Psychology and Neuroscience, Brigham Young University, Provo, UT

J. E. Lainhart , Pathology, University of Utah, Salt Lake City, UT

Background: The developmental neuropathology of white matter maturation in the autism brain is unknown. Abnormalities in functional connectivity suggest that white matter pathways may differ in autism. Structural MRI studies of autism suggest aberrant age-related changes.

Objectives: The data were collected as part of an ongoing longitudinal MRI study on brain development in autism. In this analysis, we use cross-sectional data from Time 1 to investigate age-related differences in corpus callosum neurodevelopment.

Methods: High-resolution DTI images obtained from a 3T MRI scanner were analyzed on 74 individuals with autism and 41 control subjects. Individuals were broken down into 4 age bins: young children age 3-6, older children age 7-11, adolescents age 12-17, and young adults 18+. Volume and microstructure (fractional anisotropy, mean diffusivity, and axial and radial diffusivity) were compared for the total corpus callosum and subregions.

Results: Significant group by age interaction effects were found in the total and subregional corpus callosum measures of fractional anisotropy (FA) and radial diffusivity (Dr). These effects were driven by an increase in FA and decrease in Dr with age in controls that was absent in autism. A comparison within the autism group surprisingly showed elevated FA in young children compared to older children and adults.

Conclusions: Our cross-sectional findings suggest abnormal age-related white matter developmental trajectories in the corpus callosum in autism. These results suggest early abnormal “maturation” followed by abnormal CC development. The findings indicate white matter pathology in a major interhemispheric communication pathway in autism.

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