Autism Spectrum Disorder (ASD) and Attention-Deficit/Hyperactivity Disorder (ADHD) are among the most prevalent neurodevelopmental disorders in childhood and adolescence, often associated with significant impairments in cognitive, emotional, and adaptive functioning (1–4). While traditionally considered separate diagnostic entities, recent literature has increasingly emphasized the substantial overlap between ASD and ADHD in both symptom expression and underlying neurobiological mechanisms (5–7). To better conceptualize how ASD and ADHD can co-occur, several theoretical models of comorbidity have been proposed. Antshel and Russo (7) describe three main frameworks: the splitter model, which views ASD and ADHD as distinct disorders that frequently co-occur due to partially shared etiological factors; the subgroup model, which posits that individuals with ASD+ADHD represent a specific subgroup within one or both conditions characterized by unique neurocognitive features; and the potentiation model, according to which the simultaneous presence of ASD and ADHD leads to interactive or synergistic effects, resulting in more severe or qualitatively different clinical presentations. These models highlight that comorbidity may reflect not only additive symptomatology but also interactive mechanisms shaping developmental trajectories. In parallel, increasing attention has been devoted to sensory processing characteristics in both ASD and ADHD. Sensory atypicalities are well documented in ASD and are now recognized as a diagnostic feature, often involving hyper- or hypo-reactivity to sensory input and atypical sensory seeking. However, growing evidence indicates that sensory processing differences are also highly prevalent in ADHD, particularly in the domains of tactile, auditory, and visual modulation. Recent work (8) suggests that while ASD is more often associated with pervasive sensory modulation differences, ADHD may present with context-dependent sensory regulation difficulties linked to attentional control and arousal systems. Importantly, children with co-occurring ASD and ADHD may exhibit more complex sensory profiles, potentially reflecting the interaction between atypical perceptual processing and regulatory control mechanisms. Considering sensory processing may therefore be essential for understanding the heterogeneity of ASD+ADHD presentations.

Epidemiological estimates suggest that up to 70% of children with ASD also meet criteria for ADHD, while 30–50% of those with ADHD show subclinical or clinical autistic traits (9, 10).

Despite their high co-occurrence, ASD+ADHD presentations remain poorly understood and frequently underdiagnosed. This has direct clinical consequences, including misclassification, inadequate treatment targeting, and increased burden on families and educational systems (7, 11). There is therefore a growing need to identify whether ASD+ADHD comorbidity represents a discrete neurodevelopmental phenotype or simply the additive effect of two overlapping syndromes (12). Clarifying this distinction may lead to more accurate diagnostic practices and more effective intervention strategies.

Beyond phenomenological and neurocognitive overlap, converging evidence from psychiatric genetics indicates a substantial shared genetic liability between ASD and ADHD. Large-scale genome-wide association studies (GWAS) have demonstrated significant genetic correlations between the two conditions, suggesting partially shared polygenic architectures. Recent cross-disorder genomic analyses (13; doi: 10.1038/s41588-022-01171-3) show that common variants associated with neurodevelopmental and psychiatric traits often confer risk across traditional diagnostic boundaries, including ASD and ADHD.

Moreover, emerging large-scale genomic studies (doi: 10.1038/s41586-025-0942-6) highlight how pleiotropic genetic effects influence multiple neurodevelopmental phenotypes, supporting a dimensional view of neurodevelopmental liability. Importantly, while a significant proportion of genetic risk is shared, disorder-specific genetic influences also remain, which may contribute to the heterogeneity of clinical presentations. This genetic perspective aligns with dimensional and transdiagnostic models of psychopathology and provides a biological basis for investigating ASD+ADHD as a potentially distinct or partially overlapping phenotype rather than a mere diagnostic coincidence.

From a cognitive standpoint, both ASD and ADHD are associated with executive functioning difficulties, although their profiles differ. Meta-analytic studies have shown broad Executive Functioning (EF) impairments in ASD, including difficulties in cognitive flexibility, inhibition, and planning (14–21). ADHD, instead, is typically characterized by prominent deficits in inhibitory control, sustained attention, and attentional regulation (22, 23).

Behaviorally, ADHD is more often associated with externalizing symptoms such as aggression and rule-breaking, whereas ASD tends to involve internalizing traits like social withdrawal and affective flattening (24–26).

The Child Behavior Checklist (CBCL; 27) is widely used to assess these behavioral-emotional patterns and has shown strong utility in distinguishing clinical subtypes in neurodevelopmental populations (28–33). Recent models, such as the predictive coding theory and hypo-prior hypothesis, offer neurocognitive frameworks that help explain atypical sensory and social processing in ASD, and may also be extended to comorbid presentations (32, 34–37).

Despite high comorbidity rates, ASD+ADHD presentations remain under-investigated. A key reason is historical: until DSM-5, concurrent diagnoses of ASD and ADHD were not permitted, limiting scientific inquiry. Furthermore, research has often focused on single-disorder samples, leaving comorbid profiles relatively unexplored. This has resulted in a limited understanding of whether ASD+ADHD reflects a discrete phenotype or merely the additive expression of two neurodevelopmental conditions.

aThe current study aims to systematically compare the cognitive and emotional-behavioral profiles of children with ASD, ADHD, and comorbid ASD+ADHD using two standardized tools: the Wechsler Intelligence Scale for Children – Fourth Edition (WISC-IV; 38) and the CBCL 6–18. Previous studies suggest that stronger cognitive abilities—particularly verbal comprehension and working memory—may act as protective factors for behavioral and emotional regulation in ASD and ADHD (39, 40). This provides a rationale for examining whether such associations are preserved or disrupted in ASD+ADHD comorbidity.

We hypothesize that the ASD+ADHD group will exhibit (1) significantly lower scores in working memory, processing speed, and full-scale IQ, and (2) a broader behavioral-emotional dysregulation profile, including elevated internalizing and externalizing symptoms. Furthermore, we expect that cognitive abilities will show protective associations with behavioral outcomes in the ASD and ADHD groups, but not in the ASD+ADHD group, reflecting disrupted cognitive-emotional integration in the comorbid phenotype.

Preliminary analyses on demographic variables were conducted using a one-way ANOVA and chi-square tests. The ANOVA indicated a marginal age difference among groups, F(2,204) = 3.05, p = .051, with the ASD+ADHD group being slightly younger on average. A chi-square test showed that sex distribution did not significantly differ among groups, χ²(2) = 0.80, p = .669.

The pattern observed in the ASD+ADHD group reflects a combination of ASD- and ADHD-related characteristics. Although certain group differences emerged, the overlap in cognitive performance with the ADHD group and the absence of differences in overall behavioral severity suggest that conclusions about a distinct phenotype should be drawn cautiously. Consistent with our hypotheses, the ASD+ADHD group showed lower cognitive performance than the ASD group; however, their scores did not differ significantly from the ADHD group. It is important to note that age differed slightly across groups; however, this difference was small in magnitude (approximately one year) and all WISC-IV and CBCL scores were age-standardized, reducing the likelihood that age significantly influenced the observed group differences. These findings align with prior work showing that the co- occurrence of ASD and ADHD results in amplified executive dysfunction, with medium to large effect sizes supporting their clinical relevance (14, 46–49).

Behaviorally, the ADHD group presented with prominent externalizing behaviors, such as aggression and rule-breaking, in line with disinhibition models of ADHD (22, 50, 51). The ASD group, conversely, exhibited higher levels of withdrawn/depressed traits, reflecting internalizing affective symptoms (26, 52). The comorbid ASD+ADHD group demonstrated the broadest spectrum of dysregulation, encompassing both internalizing and externalizing domains, as well as elevated scores on supplementary CBCL scales such as Sluggish Cognitive Tempo and Obsessive–Compulsive symptoms (53, 54).

One of the most striking findings is the relative absence of protective correlations between cognitive functioning and behavioral outcomes in the ASD+ADHD group, in contrast to the other two groups. While verbal and working memory skills in ASD and ADHD were significantly associated with better school functioning and fewer emotional-behavioral symptoms, these associations were diminished or reversed in the comorbid group. This dissociation may reflect a breakdown in the cognitive- emotional integration mechanisms that typically support adaptive functioning in neurodevelopmental populations (18, 40, 55).

An additional point worth considering concerns the interpretation of attentional difficulties in children with ASD, particularly those with higher cognitive abilities. Recent literature highlights the ongoing challenges in differentiating ADHD-related inattention from attentional patterns associated with ASD-related cognitive styles (56). In individuals with ASD, apparent inattention may sometimes reflect differences in information processing, selective interest, or reduced engagement with non-preferred stimuli rather than primary executive dysfunction. This distinction is clinically relevant, as it underscores the importance of integrating multiple sources of information—including clinical observation, developmental history, and neuropsychological assessment—when evaluating attentional symptoms. Such a multimethod approach may help avoid over- or under-identification of ADHD in cognitively able autistic individuals and may partly explain variability in school-related outcomes.

These results may be cautiously considered within the framework of predictive processing theories, which have been proposed to explain atypical sensory and perceptual inference in ASD (34, 36, 57). ADHD, in contrast, is characterized primarily by attentional dysregulation rather than alterations in predictive coding (58). In comorbid ASD+ADHD, the interaction between atypical perceptual inference and attentional control difficulties may contribute to challenges in behavioral and emotional regulation; however, this interpretation remains speculative and requires direct neurocognitive investigation.

This interpretation is consistent with recent findings on altered cortical connectivity and reduced error prediction in comorbid samples (59).

From a clinical standpoint, these findings underscore the necessity of recognizing ASD+ADHD comorbidity as a distinct phenotype that requires specific assessment and intervention approaches. Comprehensive evaluations should integrate cognitive testing (e.g., WISC-IV) with dimensional behavioral measures (e.g., CBCL) to capture the full range of functioning. Intervention protocols should be multimodal, combining executive function training with behavioral regulation strategies, emotional resilience building, and family psychoeducation. Importantly, approaches that capitalize on cognitive strengths—often effective in ASD—may be less generalizable to comorbid cases.

We propose a heuristic model (Figure 1) to visually represent the distinct cognitive-behavioral integration patterns across groups. In ASD, higher verbal skills buffer internalizing symptoms; in ADHD, executive deficits drive externalizing behavior. In ASD+ADHD, executive and regulatory systems appear jointly compromised, disrupting this buffering mechanism and contributing to more global dysregulation. This heuristic model can also be viewed in relation to other contemporary frameworks proposed to understand neurodevelopmental comorbidity. Recent models emphasize transdiagnostic dimensions, shared neurocognitive liabilities, and the dynamic interaction between cognitive control, emotional regulation, and environmental demands (60, 61). Within this perspective, our model aligns with dimensional approaches by highlighting both shared and disorder-specific mechanisms, while also proposing that the co-occurrence of ASD and ADHD may involve non-additive interactions that alter the typical protective role of cognitive strengths. Thus, rather than competing with existing models, the present heuristic framework may be seen as a clinically grounded complement that integrates cognitive and behavioral data at the phenotypic level.

These findings suggest that dimensional and phenotype-informed approaches may offer useful insights for understanding comorbidity, although further research with more comprehensive designs is needed before drawing firm conclusions. Future longitudinal studies are needed to explore developmental trajectories and treatment responsiveness in comorbid presentations. Integration of neurobiological, cognitive, and behavioral data will be essential to advance precision psychiatry for neurodivergent youth (36, 39, 57, 59, 62).

This study contributes to the growing body of literature emphasizing the need to conceptualize ASD+ADHD comorbidity as a distinct clinical and cognitive phenotype, rather than a simple additive overlap of two separate disorders. Children with comorbid presentations showed lower cognitive performance than the ASD group but did not differ significantly from the ADHD group, and displayed intermediate behavioural patterns across CBCL domains.

While these findings emerge from an Italian clinical sample, the observed cognitive and emotional profiles are likely relevant to broader neurodevelopmental populations, given the use of standardized, cross-culturally validated assessment tools.

Moreover, the comorbid group showed greater severity in supplementary behavioral dimensions, such as Sluggish Cognitive Tempo and Obsessive–Compulsive symptoms, which aligned more closely with the ASD phenotype. These findings suggest that comorbidity may involve both the accumulation and amplification of vulnerabilities associated with each individual disorder.

The data also confirm that verbal cognitive abilities may act as a protective factor in children with ASD, facilitating better academic adaptation and reduced behavioral difficulties, particularly in the domains of attention, emotional regulation, and social interaction. However, this protective association was markedly attenuated—or altogether absent—in the ASD+ADHD group, where cognitive performance showed limited and inconsistent correlations with emotional-behavioral outcomes. This suggests a disintegration of the regulatory role of cognitive strengths in comorbid presentations, potentially due to the simultaneous disruption of attentional control, inhibition, and predictive processing systems.

From a clinical perspective, these findings highlight the importance of early, comprehensive, and multidimensional assessment strategies—particularly for children with suspected dual diagnoses. Tailored interventions should address executive dysfunction, emotional and behavioral dysregulation, and adaptive skill development. Furthermore, capitalizing on individual cognitive strengths, where present, may support compensatory mechanisms in ASD, though such approaches may require substantial adaptation when addressing comorbid cases.

The reporting of effect sizes alongside p-values supports a more nuanced interpretation of the findings and aligns with best practices in clinical research reporting.

Future research should pursue longitudinal designs to track developmental trajectories and examine how cognitive-behavioral profiles shift over time across diagnostic groups. Neurobiological investigations—including structural and functional neuroimaging, electrophysiology, and genetic studies—may elucidate the shared and unique mechanisms underlying ASD, ADHD, and their intersection. Additionally, incorporating environmental and contextual factors (e.g., family dynamics, school supports, socio-economic status) will be essential in identifying modifiable protective factors and enhancing real-world functional outcomes.

Ultimately, embracing the complexity and heterogeneity inherent to neurodevelopmental conditions like ASD and ADHD—and their frequent comorbidity—will enhance our ability to provide individualized, evidence-based care. A precision clinical approach that considers both dimensional and categorical models of functioning is critical to addressing the diverse needs of neurodivergent individuals and their families.