1. Avolio E, Olivito I, Minervini D, Soda T, De Bartolo A, Rocca C, Alò R, Facciolo RM. Neuronutrition in ASD: Involvement of gut microbiota, oxidative stress and inflammatory markers. Neurosci Biobehav Rev;2026 (May 22);187:106775.

Autism spectrum disorder (ASD) is a neurodevelopmental disorder displaying altered human behaviors, such as social interaction impairments, stereotypical/repetitive activities and emotional dysregulation. Children with ASD are often affected by gastrointestinal problems and gut microbiota dysbiosis. Inflammation and immune dysfunction are key contributors to ASD, as shown by high proinflammatory cytokines and oxidative stress. Indeed, notable implication of the nuclear factor kappa B in the severity of ASD derives from its ability to amplify neuroinflammation. This narrative review focused attention on neuronutrition and gut microbiota manipulation for mitigation of ASD symptoms, including neuroinflammation and oxidative stress. Studies in both rodents and humans with ASD have revealed that both pure and mixed Lactobacillus and Bifidobacterium were effective in ameliorating behavioral symptoms and GABA/glutamate imbalance. Often, the combined use of probiotics and prebiotics can have greater health benefits in ASD. Additionally, dietary interventions and microbiota transfer therapies along with low-to-moderate-intensity exercise have been proposed to improve gastrointestinal and behavioral symptoms. However, despite some encouraging results, biases in the neuronutrition/microbiota literature still exist. Indeed, many studies rely on small sample sizes, cross-sectional designs, and heterogeneous populations that differ in diet, medications, and comorbidities. In this context, the development of a precision diet tailored to individual gut microbiome profiles will allow for a broader understanding of the microbial ecosystem and relative therapeutical applications. Hence, by integrating metagenomics, metabolomics, epigenomics, with evaluation of environmental and nutritional factors, it will be possible to significantly improve the quality of life for people with ASD and their families.

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2. Boccaccio FM, Klip H, Vollebregt MA, Pieters S, Rizzo R, Pirrone C, Buitelaar JK. Cognitive disengagement syndrome across attention deficit/hyperactivity disorder, autism spectrum disorder, and internalizing disorders: towards a transdiagnostic construct. Eur Child Adolesc Psychiatry;2026 (May 22)

Cognitive Disengagement Syndrome (CDS) refers to symptoms of fogginess, daydreaming, blank staring, and slowed behaviour. Growing evidence suggests that CDS reflects a transdiagnostic construct. This study aimed to examine (1) associations between age, sex, and CDS severity; (2) differences in CDS across Attention-Deficit/Hyperactivity Disorder (ADHD), Autism Spectrum Disorder (ASD), and internalizing disorders; and (3) associations between CDS and quality of life, as assessed by the KIDSCREEN-27. CDS was assessed in 958 clinically referred children and adolescents (mean age = 10.7 ± 2.8 years; 36.3% female) with a primary diagnosis of ADHD (n = 353), ASD (n = 494), or internalizing disorders (n = 111). Four Child Behaviour Checklist (CBCL) items (13, 17, 80, 102) were used to operationalize CDS. Analyses included ANOVAs, MANOVAs, and multiple regression analyses in the full sample and a subsample without comorbidities. CDS levels didn’t differ by sex, whereas adolescents (12-17 years) showed higher CDS levels than children (6-11 years). Across diagnostic groups, ASD (M = 2.6, SD = 1.8) and internalizing disorders (M = 2.6, SD = 1.9) displayed higher CDS scores than ADHD (M = 1.8, SD = 1.6; p < .001). These findings remained significant in the subsamples without comorbidities (p < .001). Multiple regression analyses indicated that higher CDS scores were significantly associated with lower quality of life (B = -2.20, p < .001), independent of diagnostic group, sex, and age, without significant interaction between CDS and diagnosis. Correlational analyses indicated stronger associations between CDS with autistic (r = .25-.36; p < .05) and affective CBCL symptom dimensions (r = .19-.36; p < .05) dimensions than with ADHD symptoms. CDS appears to represent a clinically relevant transdiagnostic construct. Its strong expression in ASD suggests that it captures disengagement mechanisms beyond current nosological frameworks.

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3. Carolyn Graff J, Oh E, Etheridge S, Fisher M, Hill L, Kent K, LaMothe J, Nelson S, Reaves RP, Betz C. Nursing standards of practice and persons with intellectual and developmental disabilities: Concepts and competencies. Nurs Outlook;2026 (May 20);74(3):102796.

BACKGROUND: Despite the publication of ANA Standards for intellectual and developmental disabilities (IDD) nursing, individuals with IDD continue to experience inequities in health care access, quality, and outcomes. PURPOSE: This study examined how 14 IDD concepts derived from legislation, policy, and self-advocacy movements are represented within the Intellectual and Developmental Disabilities Nursing: Scope and Standards of Practice (ANA, 2022). METHODS: Using a document analysis approach, nurses with expertise in IDD nursing coded competencies across eight standards for the presence of each concept. DISCUSSION: Holistic Health, Advocacy, and Lifespan were frequently represented, whereas Cultural Competence, Integration, and Systemic Change were rarely evident. These findings reveal progress and ongoing gaps between nursing standards and contemporary disability and equity principles. CONCLUSION: Strengthening the explicit integration of Equity, Inclusion, and Systemic Change can guide nursing education, policy, and leadership to advance equitable care for all persons with IDD, ultimately shaping a more inclusive healthcare workforce.

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4. Chen Y, Hawkins B, Puckett H, Sharp K, Lopez A, Zeithamova D, Xie H, Verbalis A, VanMeter AS, Gaillard WD, Kenworthy L, Vaidya CJ. From cognitive abstraction to adaptive behavior: neural bases of concept learning in autistic adolescents. Mol Autism;2026 (May 22)

BACKGROUND: Learned knowledge does not consistently generalize to new contexts in autistic individuals, limiting potential for adapting to real-world demands. This challenge is hypothesized to stem from difficulties with forming abstract representations, potentially arising from perceptual processing that favors local details over the gestalt. We tested the prediction that generalization would be primarily based on exemplar-specific representations in autistic youth using computational modelling coupled with neuroimaging. METHODS: Sixty-four autistic adolescents without intellectual disability (69% males; ages 14-18 years) completed a category generalization task during functional magnetic resonance imaging at two time points. Computational models estimated abstract (prototype-based) and specific (exemplar-based) representations and underlying neural correlates. We further examined associations with adaptive functioning and moderation by autistic traits. RESULTS: Contrary to predictions, we observed a consistent prototype-dominant majority, a subgroup who generalized without consistent representational reliance, and a small minority who failed to acquire category structure. Neural prototype correlates were observed in bilateral ventromedial prefrontal cortex (VMPFC), inferior parietal lobule (IPL), right frontal pole, and right lateral occipital cortex, while neural exemplar correlates were observed in bilateral cuneus. Better generalization predicted better real-world adaptive functioning. Moreover, greater prototype-related activation in left IPL predicted better adaptive functioning in participants with higher autistic traits. LIMITATIONS: Generalizability is limited to autistic adolescents without intellectual disability as the design did not include typically developing youth. CONCLUSIONS: These findings challenge the prevailing view that concept learning in autism relies primarily on hyper-specific perceptual processing, identify meaningful variability in representational strategies, and reveal neural pathways through which abstract representation may support real-world adaptive behavior. These findings set the foundation for exploring abstract representation as an intervention target in autism.

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5. Chow SCW, Wang Y, Leung OLK, Liang LS, Soo MT, Jalal K, Wong SCM, Lee TMC, Tso WWY. Risk of Autism Spectrum Disorder and Attention-Deficit/Hyperactivity Disorder in Children With Hypoxic-Ischemic Encephalopathy. J Autism Dev Disord;2026 (May 22)

PURPOSE: This study investigated the risk of ASD and ADHD in children who have survived hypoxic-ischemic encephalopathy (HIE), one of the common conditions during birth resulting in neonatal brain injury. METHODS: A population-based cohort study analyzed electronic medical records of term infants with HIE born in public hospital in Hong Kong from 1st January 2004 to 31st December 2018 with followed-up until 31st Dec 2024. The association of HIE with ADHD and ASD was examined using log-binomial regression models adjusting sequentially for age, sex, and socioeconomic status (SES). RESULTS: A total of 533,230 children were included of which 349 cases had a diagnosis of HIE. Compared to children without history of HIE, the RR of ADHD in children with HIE was 1.94 (CI 1.40-2.68, p < 0.001) in the unadjusted model, 1.83 (CI 1.32, 2.52, p < 0.001) when adjusting for age & sex, and 1.84 (CI 1.34, 2.55, p < 0.001) when adjusting for age, sex and socioeconomic status (SES). The relationship between ASD and HIE did not reach statistical significance, RR = 1.58 (p = 0.08, CI 0.93, 2.68) adjusted for age, sex and SES. A significant interaction effect was found between HIE and the age of mothers, the RR of ADHD was 4.25 (CI 2.14, 8.46) in mothers under 24 years of age. CONCLUSION: Children with HIE, especially those born to younger mothers, were associated with elevated risk of ADHD. The relationship between ASD and HIE remained inconclusive, suggesting the need for further research to clarify this potential association.

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6. Ciccozzi A, Murgia F, Piroli A, Paladini A, Ciccone C, Leonardis F, Fionda D, Ciccone A, Marinangeli F. Management of an Autism Spectrum Disorder (ASD) Patient With Respiratory Failure in the Intensive Care Unit: A Case Report on the Role of Dexmedetomidine. Case Rep Crit Care;2026;2026:2549155.

This clinical case describes the management, in an intensive care unit (ICU), of a patient with a severe form of autism spectrum disorder (ASD) Level 3, suffering from acute respiratory failure that evolved into acute respiratory distress syndrome (ARDS). Throughout the entire period of hospitalisation in the ICU, sedation of the patient played a key role in the performance of all invasive and noninvasive therapeutic procedures, in particular artificial ventilation and subsequent weaning, due to the underlying disorder that rendered the patient completely uncooperative. Dexmedetomidine was used during initial admission to the ICU for initial treatment, during the period of artificial ventilation and finally during weaning from mechanical ventilation. The α (2) agonist, due to its pharmacodynamic and pharmacokinetic characteristics, also facilitated the overlap with home antipsychotic drugs upon both discontinuation and reinstatement, allowing discharge from the ICU and safe and serene home management of the tracheostomy until its closure.

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7. Feng S, Li B, Ni W, Hoi SP, Li X, Zhang J, Wang Q, Chen L, Yi L. Staged Audiovisual Speech Integration and Altered Early-Stage Audiovisual Processing in Autistic Children: An EEG Investigation. Autism Res;2026 (May 22):e70273.

Autistic children exhibit difficulties in audiovisual speech integration, which are associated with their social communication challenges. The neural mechanism underlying audiovisual speech integration difficulties in autism remains unclear. We recruited 19 neurotypical (NT) children and 29 autistic children. We recorded their behavioral responses and Electroencephalography (EEG) signals to audiovisual congruent syllables, and incongruent syllables that could evoke audiovisual speech integration (i.e., McGurk effect). For the EEG analysis, we further classified autistic children into the autistic McGurk group and the autistic non-McGurk group based on their strength of audiovisual speech integration. Behaviorally, we found reduced audiovisual speech integration in autistic children. At the neural level, we found that: (1) NT children showed an early stage audiovisual processing (indexed by the N1 amplitude), which was altered in two autistic groups; (2) all three groups exhibited a successful audiovisual incongruence detection (i.e., phonological Mismatch Negativity, pMMN); (3) NT and autistic McGurk groups could successfully resolve the audiovisual incongruence (indexed by the restoration of pMMN), but the autistic non-McGurk group could not (indexed by the sustained negative amplitude). Furthermore, we found a distinct temporal decoding pattern between non-McGurk and congruent trials across groups: both NT and autistic McGurk groups exhibited early EEG decoding, whereas the autistic non-McGurk group demonstrated successful decoding during late processing stages. Audiovisual speech integration entails a three-stage process in NT children: early audiovisual processing, audiovisual incongruence detection, and audiovisual incongruence resolution. The altered early-stage processing was possibly the neural mechanism underlying the reduced audiovisual speech integration in autistic children. By employing EEG technique, we explored the neural mechanism underlying audiovisual speech integration difficulties in autism. We found that autistic groups showed an altered early‐stage audiovisual processing (indexed by an altered N1 amplitude) compared to NT children. NT group demonstrated a three‐stage process in audiovisual speech integration: early response to audiovisual incongruency, audiovisual incongruence detection, and audiovisual incongruence resolution. The altered early‐stage audiovisual processing might be seen as a neural signature of autism in audiovisual speech processing, potentially contributing to the diagnosis of autism. eng

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8. Grillo DS, de Carvalho Alencar ME, da Silva Ribeiro Souza V, Pinheiro APB, Monteiro N, de Araújo Machado RJ. Microplastics as a Silent Threat to Child Neurodevelopment: Evidence and Perspectives on Autism. Int J Dev Neurosci;2026 (Jun);86(4):e70141.

Autism spectrum disorder (ASD) is caused by an interaction of both environment and genetics. Recently, there has been an increased focus on how environmental toxins may alter a child’s biological systems. Microplastics and nanoplastics are of great interest to researchers due to their ubiquitous nature and potential to interact with the human body. Through ingestion, inhalation and dermal contact, humans can consume both sizes of particles, which may enter the blood stream and under some circumstances pass the blood-brain barrier impacting the central nervous system. Studies on exposure to microplastics indicate an increase in oxidative stress and inflammation as well as a decline in attention and memory. Smaller, nanoplastic particles appear to be able to bypass biological barriers and elicit more drastic responses. In this review, studies ranging from 2020 to 2025 focusing on microplastics exposure and neurodevelopment including the potential for impact on ASD were sought and selected based on defined criteria, of which six studies ultimately met the criteria. Currently, there is no evidence for a causal relationship between microplastic particles and ASD; however, it appears to be a potential environmental factor influencing neurodevelopment. These findings highlight the necessity for more clinical study and long-term research in this area.

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9. Haque A, Bell-Sambataro EE, Patel F, Mamilly L, Obrynba K, Ladd JM. Atypical Presentation of New Onset Diabetes with Hyperglycemic Hyperosmolar State in Two Toddlers. J Clin Res Pediatr Endocrinol;2026 (May 22);18(Suppl 1):70-74.

Hyperglycemic hyperosmolar state (HHS), or mixed HHS with diabetic ketoacidosis (DKA), is a rare complication of diabetes in children. Prompt recognition of hyperosmolality is necessary to prevent morbidity and mortality. We report two of the youngest cases with HHS, both presenting as new onset of type 1 diabetes. The first was a 3-year-4-month-old male with autism spectrum disorder who presented with glucose 76.0 mmol/L (1370 mg/dL), calculated serum osmolality 388 mOsm/kg, and trace urinary ketones, consistent with HHS and complicated by acute kidney injury. The second was a 4-year-7-month-old male with Trisomy 21 and autism spectrum disorder who presented with glucose 117.3 mmol/L (2114 mg/dL), calculated serum osmolality 401 mOsm/kg, and elevated serum β-hydroxybutyrate, consistent with mixed HHS-DKA and complicated by acute kidney injury and pancreatitis. Both received aggressive rehydration although hyperosmolality was initially overlooked, resulting in earlier and higher insulin dosing more typical of DKA than HHS. Both recovered without sequelae. In each case, young age and developmental delay likely contributed to hyperosmolality, given the inability to communicate increased thirst and freely access water. A high index of suspicion for HHS is necessary as significant rehydration and delayed start of low dose insulin infusion are recommended to prevent complications.

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10. İlçioğlu Ekici G, Kılıç BG. Predictors of psychosocial adjustment in siblings of children with autism spectrum disorder: a structural equation modeling study. Turk J Pediatr;2026 (Apr 30);68(2):297-312.

BACKGROUND: Siblings of children with autism spectrum disorder (ASD) are at increased risk of psychosocial difficulties due to altered family dynamics and parental stress. However, the mechanisms linking ASD severity, parental psychopathology, and sibling outcomes remain unclear. This study aimed to identify determinants of psychosocial problems among siblings of children with ASD using a family-systems framework and structural equation modeling (SEM). METHODS: A case-control study was conducted with 67 siblings of children with ASD (ASD-Sibs) and 67 siblings of typically developing children (TD-Sibs), aged 6-18 years. ASD severity was rated using the Childhood Autism Rating Scale (CARS). Sibling depression, anxiety, and emotion regulation were assessed using the Child Depression Inventory (CDI), Screen for Child Anxiety Related Emotional Disorders (SCARED), and Cognitive Emotion Regulation Questionnaire (CERQ). Parents completed the Child Behavior Checklist (CBCL), Beck Depression and Anxiety Inventories (BDI, BAI), and Family Assessment Device (FAD). SEM was used to examine predictors of sibling psychosocial outcomes. RESULTS: ASD-Sibs reported significantly higher depressive and anxiety symptoms than TD-Sibs. SEM revealed that maternal depression and general family functioning were significant predictors of sibling depression, anxiety, and behavioral problems. ASD severity indirectly influenced sibling outcomes through maternal depression and anxiety. Positive reappraisal emerged as a protective factor against anxiety. CONCLUSIONS: Maternal psychological well-being and family functioning are key determinants of psychosocial adjustment among ASD-Sibs. Autism severity affects siblings indirectly via maternal psychopathology, underscoring the importance of holistic, family-centered interventions to promote resilience in families of children with ASD.

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11. Karagyaur M, Averina O, Bozov K, Dzhauari S, Priymak A, Khaybullina R, Permyakov O, Popov V, Grigorieva O, Illarionova M, Shkarina L, Gulyaev M, Lebedev D, Primak A, Sergiev P, Semina E, Klimovich P, Samokhodskaya L, Malkov P, Pirogov Y, Tsygankov B, Chaika Y, Tkachuk V, Neyfeld E. Novel mouse line with D277N mutation in the Plau gene displays autism spectrum disorder-like traits. Front Cell Dev Biol;2026;14:1762737.

INTRODUCTION: Genetic technologies provide an opportunity to study the molecular basis of a wide range of hereditary pathologies, including mental disorders. Reproducing of potentially pathogenic genomic variants in cellular and animal models allows establishing their functional significance and possible mechanisms of involvement in the pathogenesis of certain disorders. METHODS: In this study, a genetic variant of urokinase type plasminogen activator (uPA, gene Plau) was modeled in mice using CRISPR/Cas genome editing tool, enabling a better understanding of the role of this molecule and its associated pathways in brain development. The protease uPA plays an important role in the directed migration of neural progenitors, glial, endothelial and immune cells, it participates in axon guidance and maturation of synaptic connections, activation of growth factors and degradation of the extracellular matrix. To study the contribution of the catalytic function of uPA to brain development, we have created for the first time a mouse line carrying the D277N (rs1243306395) mutation. We assessed social activity, anxiety, memory, problem-solving ability and stress resistance of these mice, as well as histological features of their brains. RESULTS: Timely and correct functioning of the Plau gene ensures adequate positioning of crucial cellular components in the developing nervous system. According to bioinformatic calculations, the D277N (corresponds to the human single nucleotide variant rs1243306395) substitution that happens due to C-to-T mutation in the murine Plau gene may impair the catalytic activity of the uPA protein. While retaining their ability to find solutions in the escape test, this mouse line is characterized by high levels of anxiety, impaired social behavior, slowed learning dynamics (spatial memory), and impaired adaptation to stressors. This behavioral pattern can potentially be interpreted as autism spectrum disorder Histological analysis of the brain and cerebral cortex in Plau-D277N mice revealed brain volume enlargement and cortical thickening of approximately 10-15% compared to wild-type mice. DISCUSSION: In this study, we draw attention for the first time to the genomic variant rs1243306395 in the Plau gene as a potential cause of autism spectrum disorder and propose the genetically modified Plau-D277N mouse line as a model object for studying the pathogenesis of this disorder. These models can also be used for the development and testing of promising therapeutic approaches and pharmacological agents.

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12. Kildahl AN, Halvorsen MB, Hellerud JMA, Helverschou SB. Factor Structure and Longitudinal Measurement Invariance of the Psychopathology in Autism Checklist. J Autism Dev Disord;2026 (May 22)

PURPOSE: The Psychopathology in Autism Checklist (PAC) was developed to screen for mental health disorders in autistic adults with intellectual disabilities, focusing on identifying common mental health symptoms that do not overlap with autism characteristics. The current study aims to examine the factor structure and longitudinal measurement invariance of the PAC. METHODS: Existing data from a longitudinal multicentre study of mental health treatment in autistic individuals with intellectual disabilities were used. The PAC factor structure was examined using intake data (n = 201, 60 females, aged 13-68) and the longitudinal measurement invariance was explored using data across the study’s three time points (intake, end of treatment, follow-up; n = 173, 56 females, aged 13-68). RESULTS: The four disorder-specific subscales of the PAC (psychosis, depression, anxiety, obsessive-compulsive disorder [OCD]) showed an acceptable but suboptimal fit, while the inclusion of the general adjustment problems (GAP) subscale resulted in a poorer fit. Three of the subscales (GAP, OCD, depression) showed longitudinal measurement invariance, while two did not (psychosis, anxiety), suggesting caution when using the latter subscales for evaluative purposes. An alternative model was identified, comprising 35 of the original 42 PAC items. It showed an improved fit and longitudinal measurement invariance for all five subscales across the three time points. CONCLUSION: These findings provide a starting point for further development of the PAC. While the alternative model appears to improve structural validity and seems better suited for comparisons over time, further research is needed to determine whether it could also be useful for screening purposes.

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13. Krol MA, Skodova T, Jellema T. Neural Correlates for Anticipating and Observing Goal-Directed Actions in Autism. Autism Res;2026 (May 22):e70272.

We investigated possible atypicalities in activation of cortical motor-related circuits in young adults with Autism Spectrum Conditions (ASC) and typical-development (TD) when observing others’ actions. Activation of these circuits is reflected by suppression of power in EEG-Mu oscillations (8-13 Hz). Despite strong indications for functional distinctions between the upper (10.5-13 Hz) and lower (8-10.5 Hz) Mu-subbands, their separation remained unchartered territory in ASC research. Recordings were made from central, sensorimotor and occipital areas, while goal-directed actions that varied in the extent of both social interaction and biological motion were presented in video-clips. Anticipatory Mu suppression in response to upcoming actions was found exclusively at the sensorimotor site, in both groups. That is, during the presentation of a color signal embedded in the videos, which indicated whether or not an action would ensue, significantly more Mu-suppression occurred when the signal indicated an upcoming action. No such anticipatory activity occurred at central and occipital sites. During action observation, both groups showed significantly larger Mu suppressions in (i) the lower compared to the upper Mu band, and at (ii) sensorimotor compared to occipital and central sites. Extent of social interaction and biological motion of the actions did not significantly affect responses in either group. The groups did not differ significantly from each other in either band, condition or hemisphere. At the sensorimotor site, there was an overall tendency-though no significant evidence-for less desynchronisation to observed actions, and for more synchronization to no-action events (still image), in ASC compared to TD. Immediate interpretation of others’ actions and gestures may be impaired in individuals with autism spectrum conditions (ASC). We aimed to find out whether this is related to reduced activity in representations in the brain of the visual image of others’ actions/gestures. Hereto, electrical activity was recorded from the skull of young adults with ASC (with low support needs), and from controls, while they observed actions presented in short video‐clips. During anticipation and observation of actions, both groups showed a similar level of activity. We concluded that any difficulties in ASC with interpreting others’ actions/gestures are probably not due to reduced activation of the brain’s action/gesture representations. However, it cannot be excluded that the recordings were not sensitive enough to pick‐up on subtle differences. eng

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14. Luo S, Qu S, Tan S, Song Z, Lv Y, Jia X, Tan J, Chen G, Guo H, Xia K. MSL2 disruption leads to autism-like behaviors, impairs neurogenesis, and alters histone H4K16 acetylation. Cell Mol Life Sci;2026 (May 22)

Neurodevelopmental disorders (NDDs) are frequently associated with dysregulation of epigenetic mechanisms. Recent studies have implicated variants in components of the Male-Specific Lethal (MSL) complex, including MSL2, in NDD pathogenesis. However, the pathogenic mechanisms underlying MSL2-related neurodevelopmental disorders remain poorly defined. Here, we elucidate the role of MSL2 in neurodevelopment and NDDs through comprehensive analysis of conditional knockout mice and multi-omics profiling. Aggregation of published and unpublished genomic data and case series revealed that pathogenic variants in MSL complex components, including MSL2, presented with shared phenotypes. Using a nervous system-specific Msl2 conditional knockout mouse model, we demonstrate that Msl2 deficiency leads to impaired social novelty recognition, learning deficits, and spatial memory impairments. These behavioral abnormalities are characterized by disrupted neocortical lamination, compromised proliferation capacity and differentiative ability of neural progenitor cells, and reduced neuronal migration. Mechanistically, Msl2-deficient brains exhibit significantly reduced levels of histone H4 lysine 16 acetylation (H4K16ac), particularly at promoter regions. Integrated RNA-seq, ChIP-seq, and ATAC-seq analyses revealed widespread transcriptional downregulation and loss of chromatin accessibility at NDD-related genes. Variants in the MSL2 DNA-binding domain disrupted its ability to target key regulatory genes including FMR1, confirming direct epigenetic regulation. Together, these findings demonstrate that MSL2 promotes neurodevelopment primarily by maintaining chromatin accessibility through H4K16ac deposition, and its disruption underlies the molecular and behavioral hallmarks of NDDs.

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15. Masri RM, Bayoumi MAA, Amin RI, Alsharif HOA, Musa A, Mudrek AS, Selim B, Chandra P, Elshaar S. Neurodevelopmental outcomes of children born to diabetic mothers in the Qatari population: a retrospective study. BMJ Paediatr Open;2026 (May 22);10(1)

OBJECTIVES: Maternal diabetes is linked to adverse perinatal outcomes, but its association with neurodevelopmental delays in offspring remains unclear. This study aimed to investigate the relationship between maternal diabetes and neurodevelopmental outcomes in children born to Qatari mothers. METHODS: This retrospective population-based cohort study included full-term children born in 2017 to Qatari mothers with gestational diabetes, pre-pregnancy diabetes, or no diabetes. Neurodevelopmental outcomes such as autism spectrum disorder (ASD), speech delay, and gross and fine motor delays were assessed at the age of 4 years. Data for the study were retrieved from electronic medical records. RESULTS: Of the 5141 eligible children, 1222 (23.8%) were born to mothers with gestational diabetes mellitus (GDM), 140 (2.7%) to mothers with pre-pregnancy diabetes and 3779 (73.5%) to non-diabetic mothers. Overall, 70 (1.58%) children were diagnosed with autism, 161 (3.63%) with speech delay, 44 (0.99%) with gross motor delay and 43 (0.97%) with fine motor delay. In crude analyses, children of mothers with GDM had significantly higher odds of autism (OR 1.70, 95% CI 1.03 to 2.81) and speech delay (OR 1.44, 95% CI 1.02 to 2.04) compared with controls. However, these associations were not statistically significant after adjusting for confounders (autism: adjusted odds ratio (aOR) 1.58, 95% CI 0.94 to 2.66; speech delay: adjusted odds ratio (aOR) 1.39, 95% CI 0.97 to 2.00). No significant associations were observed between maternal diabetes and gross or fine motor delays in either crude or adjusted models. CONCLUSION: Despite non-significant associations, findings highlight the role of effective diabetes management and the need for region-specific, longitudinal research on child neurodevelopment.

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16. Pérez-Sisqués L, Bhatt SU, Caruso A, Robb JL, Donovan APA, Bamford R, Torres-Cano A, Spring S, Hendy E, Gileadi TE, Panasiuk M, Trengove J, Jindal N, Ahmed MU, Sabbioni M, Taylor-Papadimitriou J, Cash D, Clifton N, Ellegood J, Andreae LC, Lerch JP, Scattoni ML, Giese KP, Fernandes C, Basson MA. Autism-like phenotypes and increased NMDAR2D expression in mice with KDM5B histone lysine demethylase deficiency. Sci Adv;2026 (May 22);12(21):eadq6577.

Loss-of-function mutations in genes encoding lysine demethylases specific for trimethylated lysine 4 of histone 3 (H3K4me3) are associated with neurodevelopmental conditions, including autism spectrum disorder (ASD) and intellectual disability (ID). To study the role of KDM5B (lysine demethylase 5B)-mediated H3K4me3 demethylation, we investigated neurodevelopmental phenotypes in mice without KDM5B demethylase activity. These mice exhibited autism-like behaviors and increased brain size. H3K4me3 levels and the expression of neurodevelopmental genes were increased in the developing Kdm5b mutant neocortex. Increased H3K4me3 levels at the promoter and associated expression of the Grin2d gene were associated with increased levels of N-methyl-d-aspartate receptor subunit 2D (NMDAR2D) protein in synaptosomes isolated from the early postnatal Kdm5b-deficient neocortex. Treating mice with the NMDAR antagonist memantine rescued deficits in ultrasonic vocalizations. These findings suggest that increased H3K4me3 levels and associated Grin2d gene up-regulation disrupt brain development and function, leading to socio-communication deficits and identify a potential therapeutic target for neurodevelopmental disorders associated with KDM5B deficiency.

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17. Ragalmuto FGM, Oranje B, Ziermans T. Basic sensory risk markers characteristic of schizophrenia in autism spectrum disorder: A systematic review and meta-analysis. Neurosci Biobehav Rev;2026 (May 20);187:106764.

AIMS: Neurophysiological impairments in basic sensory processes are a hallmark feature in schizophrenia (SZ) and are commonly reported in individuals at-risk of developing SZ. Autism spectrum disorder (ASD) is linked to a higher incidence of later psychotic disorders, including SZ. However, it remains unclear whether basic sensory risk markers for SZ are equally characteristic of ASD. METHODS: We performed a systematic review and subsequent meta-analyses of basic sensory risk markers for SZ in ASD. Following PRISMA guidelines, we included 44 studies, investigating prepulse inhibition of the startle reflex (PPI), P50 suppression, mismatch negativity (MMN), N100, and P200 amplitudes. Meta-analyses were conducted for measures with data from ≥ five studies using comparable methodology. RESULTS AND CONCLUSIONS: Patient groups were predominantly male (∼80%) with a mean age of 15.6 years. Findings were mixed, with high heterogeneity in all parameters except %PPI and startle amplitude. PPI, P50 suppression, and MMN qualified for meta-analyses, which revealed significant reductions in duration MMN and P50 amplitude to the first stimulus of paired-click paradigms. Although variability in methods precluded meta-analysis, most visual oddball studies reported significantly increased N100 amplitudes in ASD compared to controls, opposite to the decreased N100 amplitude typically observed in SZ. Coupled with preserved %PPI in ASD, these findings suggest that the N100 ERP and PPI may help differentiate between the two conditions. Simultaneously, other SZ-linked risk markers appear in ASD, and heterogeneity across samples suggests potential neurophysiological subgroups. Future research should apply standardized paradigms in sex-balanced, age-appropriate cohorts to clarify their clinical relevance.

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18. Shelley L, Pearson E, Tarver J, Waite J. Understanding Aggression in SATB2-Associated Syndrome: A Mixed-Methods Study Exploring Caregiver Perspectives. J Appl Res Intellect Disabil;2026 (May);39(3):e70247.

BACKGROUND: SATB2-associated syndrome (SAS) is a neurodevelopmental condition characterised by developmental delay, speech impairment, and craniofacial anomalies. High rates of aggression are reported in SAS, yet the profile and contributing factors remain poorly understood. This study explored caregiver perspectives on aggression in SAS. METHODS: Caregivers of 37 individuals with SAS (M age = 11.42 years) completed questionnaires on adaptive ability, aggression and behavioural function. Semi-structured interviews with 34 caregivers explored contextual factors such as triggers, co-occurring emotions, and management strategies. RESULTS: Aggression was reported in 87% of individuals, with frequent forms including pulling/grabbing (84%) and hitting with a body part (69%) or object (53%). Aggression was often linked to frustration, anxiety, and triggers relating to demands, routines, repetitive behaviour, and tangibles. Caregivers described varied management strategies and background factors influencing aggression. CONCLUSION: Findings provide the first detailed description of aggression in SAS, highlighting vulnerabilities to guide tailored behavioural assessment and interventions. People with SATB2‐associated syndrome (SAS) may show ‘aggressive’ behaviours, such as pulling, grabbing, or hitting others. Aggression is commonly linked to frustration, anxiety, and triggers like demands, changes in routines, repetitive behaviours, or accessing specific items. Caregivers use a range of strategies to manage aggression, while few individuals with SAS use their own strategies to calm or regulate themselves. These findings improve understanding of aggression in SAS and can help families, clinicians, and researchers provide more personalised support and interventions. eng

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19. Viscomi MP, Ziętek MM, Winiarczyk D, Sampino S. Placental lipid droplets and histone marks reveal a metabolic-epigenetic phenotype in the BTBR mouse model of autism. Placenta;2026 (May 20);181:184-193.

INTRODUCTION: The placenta shapes fetal brain development through metabolic and epigenetic regulation. The BTBR T(+) Itpr3(tf)/J (BTBR) mouse provides a valuable model of neurodevelopmental vulnerability. This study investigates the cellular and spatial distribution of lipid metabolic and epigenetic alterations within the BTBR placenta. METHODS: We analyzed mid-gestation (12.5 days post coitum) placentas from BTBR and control (C57BL/6J) mice. Using three-dimensional confocal microscopy and immunohistochemistry, we quantified lipid droplet (LD) architecture, the distribution of the phospholipase PLA2G4E, and specific histone modifications (H3K9 butyrylation and H3K4 trimethylation). RESULTS: Trophoblast giant cells in BTBR placentas exhibit a marked shift toward smaller lipid droplets, indicating altered lipid remodeling and fragmentation without a reduction in total lipid storage capacity. PLA2G4E displayed conserved, compartment-specific localization across placental layers. At the chromatin level, BTBR placentas showed increased H3K9 butyrylation in trophoblast giant cells and decidua, alongside decreased H3K4 trimethylation in the junctional zone and labyrinth compared to B6 placentas. These integrated metabolic and epigenetic alterations converge primarily within trophoblast giant cells. CONCLUSION: These findings define a metabolic-epigenetic placental phenotype in the BTBR mouse and support a model in which altered lipid droplet remodeling is associated with distinct chromatin states in key placental cell populations.

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20. Webb L, Chatterjee A, Holingue C, Jackson DB. Police Stops Among Adolescents With Intellectual and Developmental Disabilities: Implications for Traumatic Stress. J Autism Dev Disord;2026 (May 22)

PURPOSE: The present study examines differences in police stops, features of those stops, and stress outcomes between youth with and without intellectual and developmental disabilities (IDD). METHODS: Data from Wave 6 (age 15) of the Future of Families and Child Wellbeing Study (FFCWS), a national sample of urban-born youth in the U.S., was analyzed in 2025 (n = 3,444). Logistic regression models first examined associations between IDD diagnosis and direct police stops. Negative binomial regressions and linear regressions were then conducted among the subsample of youth who reported a direct police stop (n = 918) to examine the associations between IDD diagnosis and officer intrusiveness, perceptions of procedural justice, emotional distress during the direct stop, and police-initiated post-traumatic stress (PI-PTSS). RESULTS: Youth with IDD diagnoses did not have significantly greater odds of experiencing a direct police stop than youth without IDD. However, among youth with a direct police stop, youth with IDD diagnoses reported higher emotional distress during direct police stops and higher PI-PTSS than youth without IDD. CONCLUSION: These findings indicate that direct police stops may have more detrimental effects on stress and mental health of youth with IDD compared to youth without IDD. Policy reform, officer training, and additional research are needed to safeguard the mental health and wellbeing of youth with IDD.

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21. Zhang Z, Zhang C, Zhang X, Zhang J, Xu Y, Dou W, Li M, Zheng W, Li B. White matter structure-function coupling in neonatal brain and its association with Autism-related traits in early childhood. Transl Psychiatry;2026 (May 22)

The neonatal brain undergoes a rapid maturation of white matter pathways, yet how structural refinement within these tracts drives concurrent functional reorganization remains poorly understood. Using multimodal MRI data from 399 infants (348 term-born and 51 preterm-born) from the Developing Human Connectome Project, here we characterize the developmental trajectories of white matter structure-function coupling (SFC) and examine its associations with myelination (indexed by the T1w/T2w ratio), prematurity, and later autism-related traits. We find that SFC strength and its temporal variance develop heterogeneously across major fiber tracts, in which the inferior longitudinal and inferior fronto-occipital fasciculi exhibit a marked left-lateralized tendency, supporting the formation of nascent language and social cognition. The association between SFC and myelination is also dynamic, weakening over time in most tracts but strengthening selectively in the inferior longitudinal fasciculus. Preterm infants exhibit significantly reduced SFC across most tracts compared to term-born peers. Notably, reduced SFC in the right corticospinal tract partially mediates the association between prematurity and higher autism-related traits at 18 months. Furthermore, neonatal SFC predicts these traits only in preterm infants. These findings delineate a dynamic, tract-specific interplay between structure and function in early-life brain and establish neonatal SFC as a key link between prematurity and subsequent neurodevelopmental risk.

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