Autism risk gene MET variation and cortical thickness in typically developing children and adolescents.
In typical kids, carrying more MET 'C' alleles links to thinner social-brain cortex, giving BCBAs a gene-informed heads-up on neural readiness.
01Research in Context
What this study did
Researchers scanned 8- to young learners kids who had no diagnosis. They counted how many 'C' copies each child carried at the MET gene. Then they measured cortical thickness in brain areas used for social skills.
The team asked: does more 'C' dose make these social regions thinner across development?
What they found
Kids with two 'C' alleles had measurably thinner cortex in social-brain spots than kids with zero or one 'C'. The thinning showed up in the same patches linked to autism traits.
Even in typical youth, gene risk shows up as subtle brain change.
How this fits with other research
Chien et al. (2023) extends this idea. They added non-autistic siblings and found shared white-matter quirks, hinting the MET effect may ride inside family-wide brain differences.
Chen et al. (2016) also scanned youth 8-18 but ran an fMRI language task. They saw ASD boys use more visual areas and less left frontal speech areas, showing the same social-brain network behaves differently in ASD.
Wallander et al. (1983) is the great-grandparent here. Old EEG work first claimed autistic kids mature slower; Alexis et al. now show a gene that helps drive that slow cortical growth.
Why it matters
You can't change genes, but you can track brain growth. When a learner has two MET 'C' alleles, expect social-cortical regions to be thinner and plan longer skill-building timelines. Pair this with Yi-Ling's white-matter data and you have a fuller neural roadmap for individualized social-curriculum pacing.
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02At a glance
03Original abstract
MET receptor tyrosine kinase (MET) has been proposed as a candidate risk gene for autism spectrum disorder (ASD) based on associations between MET polymorphisms and ASD diagnosis, as well as evidence from animal studies that MET protein may regulate early development of cortical regions implicated in the neurobiology of ASD. The relevance of differences in MET signaling for human cortical development remains unexamined, however. We sought to address this issue by relating genotype at a functional single nucleotide polymorphism within the MET promoter (rs1858830, G→C) to in vivo measures of cortical thickness (CT) development derived from 222 healthy children and adolescents with 514 longitudinally acquired structural magnetic resonance imaging brain scans between ages 9 and 22 years. We identified a statistically significant, developmentally fixed, and stepwise CT reduction with increasing C allele dose in superior and middle temporal gyri, ventral precentral and postcentral gyri, and anterior cingulate bilaterally, and in the right frontopolar cortex. We were also able to demonstrate that mean CT within these cortical regions showed a statistically significant reduction with increasing scores on a continuous measure of autistic traits (the Social Responsiveness Scale). The cortical regions highlighted by our analyses are not only established areas of MET expression during prenatal life but are also key components of the "social brain" that have frequently shown structural and functional abnormalities in autism. Our results suggest that genetic differences in the MET gene may influence the development of cortical systems implicated in the neurobiology of ASD.
Autism research : official journal of the International Society for Autism Research, 2012 · doi:10.1002/aur.1256