Autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD) are among the most common neurodevelopmental conditions in children. While traditionally treated as distinct disorders, growing evidence suggests that they may share underlying biological mechanisms. A new study from the Child Mind Institute reveals that the severity of autism symptoms—rather than the diagnostic label itself—aligns with specific patterns of brain connectivity and gene expression observed across both conditions.
Overlapping Symptoms Between Autism and ADHD
ASD and ADHD frequently co-occur, blurring traditional diagnostic boundaries. Research indicates that up to 80% of children with autism also meet the criteria for ADHD, while approximately 30% of children with ADHD display autistic traits. Despite this overlap, diagnostic frameworks such as the DSM-5 and ICD-11 continue to categorize them as separate conditions.
Dr. Adriana Di Martino, research director for the Autism Center at the Child Mind Institute, explained, “We see in the clinic that some children with ADHD share symptoms qualitatively similar to those observed in autism, even if they do not fully meet the diagnostic criteria for ASD.”
Previous neuroimaging and genetic studies have suggested that ASD and ADHD may share structural and functional brain alterations, as well as overlapping genetic risks. However, results have been inconsistent due to small sample sizes, mixed symptom assessments, and reliance on parent-reported questionnaires rather than standardized clinician evaluations.
A New Approach: Linking Symptom Severity to Brain Biology
The recent study approached the question from a dimensional perspective, examining whether autism symptom severity, instead of diagnostic category, corresponds to identifiable patterns in brain connectivity and gene expression.
The study included 166 verbal children aged 6–12 years—63 diagnosed with ASD and 103 with ADHD—carefully matched for intelligence, age, and demographic factors. Using resting-state functional MRI, which measures spontaneous brain activity at rest, the team applied multivariate distance matrix regression to explore whether connectivity patterns across the whole brain correlated with individual symptom severity. This data-driven, whole-brain approach minimized bias from preselected regions.
Autism symptoms were assessed using the Autism Diagnostic Observation Schedule (ADOS-2), while ADHD symptoms were measured via the Kiddie Schedule for Affective Disorders and Schizophrenia. The researchers also mapped the brain connectivity data onto gene-expression profiles from the Allen Brain Atlas to investigate links between observed neural patterns and genes associated with both ASD and ADHD.
Key Findings: Hyperconnectivity and Shared Genes
Across all children, greater autism symptom severity corresponded with stronger communication between the frontoparietal network, which governs executive control, and the default mode network (DMN), involved in social and self-referential thought. Normally, these networks become more distinct as the brain develops, but in children with higher autism symptom severity, this “hyperconnectivity” persisted.
Additionally, these children displayed reduced separation between the DMN and other brain systems involved in attention and visual processing. Notably, ADHD symptom ratings did not correlate with brain connectivity patterns, suggesting that autism traits drive the shared biological signature.
Gene-expression analysis revealed enrichment of genes linked to neural growth and projection, many of which have been implicated in both ASD and ADHD. These findings suggest a biological dimension underlying overlapping behavioral traits, rather than strict categorical differences between diagnoses.
Implications for Understanding Neurodevelopmental Disorders
The study supports a dimensional model of neurodevelopmental conditions, emphasizing symptom severity over categorical labels. “By focusing on shared brain–gene expression patterns linked to autism symptoms across both ASD and ADHD, we can point towards a shared biological basis of these clinical observations,” Dr. Di Martino said. This approach could inform the development of biological markers for autism symptom severity and guide more personalized assessment and treatment strategies.
Conclusion
While the study benefits from objective, clinician-rated autism assessments and rigorous data-driven analysis, it has limitations. The sample size, though substantial for neuroimaging research, remains modest for genetic analyses. Most participants were male, limiting generalizability, and the genetic mapping relied on adult brain data rather than real-time developmental measures. Furthermore, standardized observational tools for ADHD equivalent to the ADOS-2 do not currently exist, possibly reducing sensitivity to ADHD-specific brain patterns.
Future research could extend these findings to other symptom domains, such as attention and emotional regulation, and track children longitudinally to observe developmental changes. Incorporating direct measures of gene expression from blood samples and recruiting more diverse populations would strengthen and validate the conclusions.
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