Pubmed (TDAH) du 29/08/26
1. Herrera T, Hyman S, Newman R, Dickerson AS, Quirós-Alcalá L, Bennett DH, Oh J, Huerta-Montañez G, Titus AR, Díaz I, Watkins DJ, Trasande L, Baker BH, Ferrara A, Cassidy-Bushrow AE, Hazlehurst M, Ghassabian A. Prenatal exposure to a mixture of non-persistent endocrine-disrupting chemicals and attention and hyperactivity symptoms in children in the ECHO cohort. Environ Int. 2026; 215: 110488.
OBJECTIVE: To examine the association between prenatal exposure to a mixture of EDCs and attention-deficit/hyperactivity disorder (ADHD) symptoms in children. METHODS: Participating were mother-child pairs from the Environmental influences on Child Health Outcomes (ECHO) Cohort (n = 3,962, 18 Sites, 2001-2021). Maternal spot urine samples collected during pregnancy were sent to the Wadsworth Center Human Health Exposure Analysis Resource laboratory and analyzed using a single assay workflow. From those samples, 24 urinary metabolites of EDCs with detection frequency > 70%, were grouped as molar sum of high- and low-molecular-weight phthalates, polycyclic aromatic hydrocarbons, bisphenol S, organophosphate esters, and organophosphate and pyrethroid pesticides. Child ADHD symptoms were assessed using raw scores from the Child Behavior Checklist for preschool-aged (CBCL/1½-5) and school-aged (CBCL/6-18) Attention-Deficit/Hyperactivity Problems subscale. Scores ≥ the 85th and 95th percentiles were respectively classified as borderline and clinical thresholds. Quantile g-computation estimated the expected change in ADHD outcome associated with a one-quartile increase in all prenatal EDC mixture concentrations, using negative binomial models for raw scores and binomial models for percentile thresholds. RESULTS: Prenatal exposure to the EDC mixture was not associated with child ADHD symptoms in preschool-aged or school-aged children in adjusted models for either continuous raw scores or percentile thresholds. CONCLUSION: Overall our findings on prenatal EDC mixture exposure and ADHD symptoms were not robust to full adjustment. Future research that can delineate factors such as windows of vulnerability and trajectories of ADHD-related symptoms may help clarify mixed findings in the literature.
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2. Mittenberg AG, Belskaya AD, Shabelnikov SV, Fesenko ZS, Sylko PA, Gainetdinov RR, Volnova AB, Vaganova AN. Comparative Proteomic Analysis of the Striatum in Heterozygous and Null DAT Knockout Rats. Int J Mol Sci. 2026; 27(17).
Deregulation of striatal neurotransmission is a key pathogenetic mechanism in neurodevelopmental disorders such as attention deficit hyperactivity disorder (ADHD) and autism. In the present study, we applied a proteomic approach to demonstrate shifts in striatal protein expression in rats with heterozygous (DAT-Het) and homozygous (DAT-KO) dopamine transporter (DAT) gene knockouts. These animals model dose-dependent ADHD- and autism-like behaviors, ranging from slightly increased activity and social disturbances in DAT-Het rats to a pronounced phenotype in DAT-KO rats. We revealed pronounced changes in the proteomic profiles of both groups, associated primarily with deregulation of proteins involved in energy and carbon metabolism. Furthermore, we identified changes in vesicular transport proteins specific to DAT-KO and DAT-Het rats. Since these changes involved SNARE complex components, we evaluated SNARE mRNA expression in our models and public transcriptomic data for mouse models of neurodevelopmental disorders, including Mbd5 gene haploinsufficiency and a polygenic model of ADHD. No significant changes in mRNA levels were revealed in any model. Thus, the identified protein expression changes likely depend on post-transcriptional mechanisms. These data suggest a deregulation of metabolism in DAT-Het rats, which becomes more pronounced in DAT-KO rats.
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3. Roberts E, Patel D, Tyagi H. Autism and attention-deficit/hyperactivity disorder traits as predictors of tic phenomenology in children and adolescents. Eur Child Adolesc Psychiatry. 2026.
The co-existence of autism and attention deficit/hyperactivity disorder in tic disorders is a key factor influencing clinical decision-making. Given the shared clinical features and a potentially overlapping aetiology, the need to identify specific tic characteristics associated with these conditions remains. The current study subsequently sought to identify tic phenomenology uniquely predicted by autism and attention deficit/hyperactivity disorder traits in children and adolescents. Data from 473 5-16-year-olds from the 2004 British Child and Adolescent Mental Health Survey with motor and/or vocal tics were used. Regression analyses were conducted to determine the effect of autism and attention deficit/hyperactivity disorder traits on: (i) the presence of motor and/or vocal tics, (ii) tic onset age, (iii) nocturnal tic expression, (iv) self-regulatory control over tic expression, (v) tic frequency during restful/low arousal state, and (vi) rebound tic activity post-suppression, before and after adjustment for confounders. Autism is associated with earlier onset of tics by approximately 2.43 years. Attention deficit/hyperactivity disorder traits are associated with a 2.64x odds of experiencing worsening tics following periods of suppression. Neither autism or attention deficit/hyperactivity disorder traits were specifically associated with motor and/or vocal tics, self-regulatory control over tic expression, nocturnal tic expression, or tic frequency during restful/low arousal states. Comorbid neurodevelopmental traits not only co-occur with tic disorders but actively shape their clinical expression and trajectory. Clinically, earlier support for autistic children with tics may facilitate a timely intervention. Intervention plans for individuals with attention deficit/hyperactivity disorder traits should consider heightened vulnerability to tic rebound post-suppression.
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4. Sahin B. Off-Time Puberty in Autism Spectrum Disorder and ADHD: A Scoping Review of Pubertal Timing, Social Cognition, and Psychopathological Risk. Res Child Adolesc Psychopathol. 2026; 54(5).
Off-time pubertal development defined as pubertal onset or progression deviating meaningfully from age- and sex-matched normative expectations confers heightened risk for internalizing and externalizing psychopathology during adolescence. Children and adolescents with neurodevelopmental disorders (NDDs), including autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD), carry pre-existing impairments in theory of mind (ToM) the capacity to represent and respond to the mental states of others that substantially compromise their capacity to navigate the increasingly complex social demands that puberty introduces. Evidence indicates that ASD is associated with elevated rates of precocious puberty and altered pubertal tempo, and that ADHD in females is linked to earlier pubertal onset with consequent internalizing symptom exacerbation; yet the mechanisms connecting pubertal timing, ToM impairment, and psychopathological risk in these populations have not been systematically reviewed. This scoping review, guided by the PRISMA extension for Scoping Reviews (PRISMA-ScR), synthesises evidence from 19 studies (2016-2026) examining pubertal timing in ASD and ADHD, the neurobiological mechanisms linking puberty to social cognition, and the clinical and psychopathological consequences of their convergence. We identify three mechanisms through which off-time puberty and pre-existing ToM impairment interact: (1) demand-capacity mismatch amplification, (2) masking and camouflaging under elevated social load, and (3) physical-cognitive developmental asynchrony. No primary studies have directly examined the moderating role of ToM on the puberty-psychopathology relationship in NDD populations, representing a critical research gap. We propose a dual-vulnerability framework and outline research priorities for future longitudinal and intervention studies in this underserved population.
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5. Salehpour F, Gonzalez-Lima F. Functional Impairments and Adverse Outcomes Associated with ADHD: A Literature Review. Medicina (Kaunas). 2026; 62(9).
Background and Objectives: Attention-deficit/hyperactivity disorder (ADHD) is increasingly recognized as a lifespan neurodevelopmental condition with far-reaching consequences for functioning and health that extend well beyond its core signs and symptoms. This narrative review synthesizes evidence on the real-world impact of ADHD across the lifespan, with a focus on academic and occupational outcomes, interpersonal and family functioning, risk-taking and behavioral outcomes, accidental and sport-related injuries, physical and medical health burdens, substance use disorders, sexual health risks, and mortality. Materials and Methods: A structured search of PubMed, Scopus, and Web of Science supplemented by reference-list screening was conducted to identify relevant clinical studies, epidemiological studies, longitudinal investigations, systematic reviews, and meta-analyses published between 2000 and 2025. Evidence was synthesized narratively, with greater interpretive weight given to systematic reviews and meta-analyses, large epidemiological datasets, longitudinal studies, and investigations accounting for important potential confounding factors. Results: Findings indicate that ADHD is associated with substantial impairments across functional, behavioral, and health domains. However, the strength and magnitude of these associations vary and may be influenced by symptom presentation, neurocognitive characteristics, psychiatric comorbidities, lifestyle behaviors, and broader clinical and contextual factors, with evidence of bidirectional relationships for some outcomes. These findings caution against uniformly interpreting adverse outcomes as direct causal consequences of ADHD and support interconnected neurocognitive, reward/motivational, emotional, and environmental pathways linking ADHD features with downstream impairment. Clinically, the evidence underscores the importance of assessing functional impairment alongside ADHD signs and symptoms. Conclusions: Overall, ADHD is associated with substantial and heterogeneous burdens across the lifespan, highlighting the need for multidimensional assessment, further longitudinal and mechanistic research, and timely access to evidence-based interventions.