Maggie L. Chow, Ph.D., from the University of California San Diego in La Jolla, and colleagues examined whole-genome messenger RNA levels and copy number variations in the prefrontal cortex of 33 autistic and control postmortem brain samples.
The researchers found that, in young patients with autism (2 to 14 years old), there were abnormalities in pathways responsible for cell number, cortical patterning, and differentiation. In contrast, in older patients with autism (15 to 56 years old) there were abnormalities in pathways responsible for signaling and repair. In DNA derived from the prefrontal cortex, there were autism-specific copy number variations seen in genes regulating cell cycle; in genome-wide association study datasets these genes were significantly associated with autism.
"Our results suggest that copy number variations and age-dependent gene expression changes in autism may reflect distinct pathological processes in the developing versus the mature autistic prefrontal cortex," Chow and colleagues conclude.
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