The researchers examined the brains of toddlers, aged one to three, using diffusion tensor imaging (DTI). Sixty-one of the toddlers were at-risk for and eventually diagnosed with ASD. Thirty-three toddlers comprised the control group. The researchers mapped the children’s nerve tracts, focusing on the tracts that connect the frontal lobe to brain regions involved in social, emotional, and language functions. A year after the study, the researchers conducted a follow-up DTI test with 14 of the children with ASD and 13 of the controls.
The children with ASD had denser nerve tracts than the controls. One and two year olds who were later diagnosed with ASD had denser and thicker nerve tracts in frontal brain regions than the controls, indicating that children with ASD have an excess of axons in their neural pathways. Toddlers with thicker, denser nerve tracts also had more social and communication deficits at the time of diagnosis than toddlers with thinner nerve tracts.
As the children approached ages three and four, their nerve tracts did not remain denser than those of controls. Although their nerve tracks thickened with age, they were slightly thinner than the controls’ nerve tracts. This suggests that, while the nerve tracts are initially over-crowded, the tracts lose function over time and do not develop properly.
The nerve tracts most affected by abnormal neural density were those connecting the frontal lobe and the uncinated fasciculus and the frontal and temporal lobes to the accurate fasciculus. These affect the brain’s emotional and linguistic areas, respectively.
The results suggest that an early overgrowth of neuronal pathways contributes to ASD. The researchers caution against using this as a biomarker for identifying ASD because the differences between children with ASD and children without ASD are relatively small. However, the findings may help researchers understand the causes of ASD.
This research is published in the journal Biological Psychiatry.
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