The neuroanatomical substrates of autism and ADHD and their link to putative genomic underpinnings.
Lisa M Berg, Caroline Gurr, Johanna Leyhausen and 17 others
PMID 37794485WHAT IT FOUND
Brain scans show autism and ADHD have distinct structural signatures, but co-occurring ADHD significantly changes the cortical thickness patterns in autistic individuals.
These anatomical differences align with genes linked to autism development, not ADHD risk genes.
Key findings
01Autism and ADHD are associated with different patterns of cortical thickness and surface area, suggesting separable neuroanatomical underpinnings.
02Co-occurring ADHD modulates the neuroanatomy of autism, with autistic individuals plus ADHD showing significantly thinner cortex in the left precentral gyrus compared to those with autism alone.
03The spatial patterns of these brain differences are enriched for genes associated with autism, but not for ADHD risk genes.
STILL TO COME
How it was doneWhat they found
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What it does not show
The ADHD only group was very small (n=25), limiting the generalizability of findings specific to ADHD without autism. ADHD status was based on symptom counts from a rating scale rather than a clinical diagnosis, which may not capture the full clinical picture. The study used a categorical design, which does not account for the dimensional nature of ADHD symptoms or the heterogeneity within autism. Gene expression data came from adult donors, which may not accurately reflect developmental trajectories in children and adolescents. Effect sizes for neuroanatomical differences were small, reflecting high individual variability within diagnostic groups.
Declared interests
The study was supported by the EU-AIMS Longitudinal European Autism Project (LEAP) and the Innovative Medicines Initiative 2 Joint Undertaking. The authors declared no competing interests.
The easy way to misread this
Do not interpret these brain structure differences as diagnostic tools or evidence of causality. The study shows group-level statistical associations, not individual markers, and cannot determine whether the brain differences cause the symptoms or result from them.