1. Binte Mohd Ikhsan SN, Holt R, Man J, Parsons T, Schalbroeck R, Ruigrok A, Baranger A, Allison C, Doherty M, Van den Bosch K, Terčon J, Violland P, Ghosh A, Cusack J, Baron-Cohen S. Access to services for autistic people across Europe. Mol Autism;2025 (Jun 14);16(1):35.

BACKGROUND: Autistic communities in Europe continue to face difficulties accessing services despite increasing rates of autism diagnosis in recent years. METHODS: To investigate autistic people’s access to services in Europe and reasons for unsuccessful access, we conducted the ACCESS-EU survey comprising of 2322 formally diagnosed autistic people and family carers living within the European Union (EU) and the United Kingdom (UK). The survey also examined age group (adult vs. child) and gender (male vs. female) differences in results. RESULTS: Overall, autistic people reported access to therapy (33.38%), mental health (29.89%), educational (27.05%), medical (34.28%), financial (26.66%), needs assessment (14.90%), information/referral (14.73%), social care (14.43%), employment (7.54%), housing (6.80%), legal (3.96%), helpline (3.40%) and other services (0.26%), and most (≥ 57.61%) had waited up to 6 months from referral to access most services. Several respondents were also unable to access therapeutic (13.53%), mental health (11.90%), autism diagnostic (5.92%), needs assessment (8.32%), financial (9.62%), educational (8.10%), social care (7.39%), information/referral (6.14%), medical (7.28%), housing (5.92%), employment (5.43%), legal (3.42%), and helpline services (2.34%). Reasons cited by respondents for their unsuccessful service access included service unavailability (23.08%), service unsuitability or participant ineligibility (20.04%), long waitlists (17.42%), service unaffordability (11.80%), and rejection from service due to autism diagnosis (9.87%), along with other reasons not listed in the survey (18.42%). Significant age group and gender differences were observed for successful access to services, waiting time, unsuccessful access and reasons for unsuccessful access. Among the five most represented countries in the survey-the UK (33.33%), Spain (14.04%), Poland (13.87%), France (11.07%) and Germany (6.03%)-overall service access was most inconsistent in Poland and the UK, highest in Germany and Spain but poorest in France. LIMITATIONS: Issues related to survey presentation such as the languages in which the survey was conducted and the phrasing of some questions should be considered, as well as issues regarding subjectivity and ambiguity of data analysis such as translation of non-English responses into English. CONCLUSIONS: Our findings suggest that service access among autistic people in Europe is inconsistent. Significant improvement to current policies is required to enhance access to services across Europe.

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2. Eissa N, Jayaprakash P, Aljneibi S, Alsaadi A, Alzaabi S, Łazewska D, Karcz T, Kieć-Kononowicz K, Sadek B. Mitigating effects of H3 receptor antagonism on cerebellar autophagic pathways and behavioral phenotypes in BTBR T+ tf/J mouse model of autism spectrum disorder. Eur J Pharmacol;2025 (Jun 15);997:177481.

Accumulation of evidence suggested the involvement of autophagic pathways and their associated AktmTOR (mammalian target of rapamycin) signalling cascade in the pathogenesis of autism spectrum disorder (ASD). Histamine 3 receptors antagonism may be neuroprotective in ASD, as this antagonism modulates autophagy which is reported to be impaired in ASD. Therefore, the effects the novel H3 receptor antagonist E169 (2.5, 5, and 10 mg/kg, i.p.) on short-term memory (STM), long-term memory (LTM), and anxiety level in male Black and Tan BRachyury (BTBR) mice were evaluated using Novel object recognition test (NORT) and open field locomotor (OFT) tests respectively. In NORT, E169 (2.5 mg/kg, i.p.) significantly improved the memory of tested BTBR mice, and the effects of E169 were similar to those of the reference mTOR inhibitor rapamycin, and were reversed following co-administration with the centrally penetrant H3 receptor agonist (R)-α-methylhistamine (RAMH). Furthermore, E169 enhanced the BTBR memory by inhibiting H3 receptors and regulating the extent of disruption in the expression of cerebellar Akt, mTOR, and LC-3 proteins of treated mice. Moreover, E169 (2.5 mg/kg, i.p.) restored the disturbed anxiety levels and hyperactivity observed in OFT. In summary, the findings indicate that H3 receptor antagonists like E169 could play a role in simultaneously regulating disrupted brain neurotransmitters and the dysregulated cerebellar Akt-mTOR signaling pathway associated with autophagy in neurological diseases. Therefore, activation of cerebellar autophagy represented by H3 receptor antagonist E169 may serve as an effective pharmacological therapeutic target for the ASD-like behavioral phenotypes and may add new therapeutic management strategy for the multifactorial disorder ASD.

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3. Fan XR, Zuo XN. Precision Neuromodulation on Amygdala-Cortical Circuits for Autism Spectrum Disorder Intervention. Biol Psychiatry;2025 (Jun 15);97(12):1108-1110.

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4. Gardner RM, Brynge M, Sjöqvist H, Dalman C, Karlsson H. Maternal Immune Activation and Autism in Offspring: What Is the Evidence for Causation?. Biol Psychiatry;2025 (Jun 15);97(12):1127-1138.

The maternal immune activation hypothesis has gained attention over the past 2 decades as a potential contributor to the etiology of autism. This hypothesis posits that maternal conditions associated with inflammation during pregnancy may increase the risk of autism in offspring. Autism is highly heritable, and causal environmental contributors to autism largely remain elusive. We review studies on maternal conditions during pregnancy, all associated with some degree of systemic inflammation, namely maternal infections, autoimmunity, and high body mass index. We also review studies of inflammatory markers in biological samples collected from mothers during pregnancy or from neonates and their relationship with autism assessed in children later in life. Recent reports indicate familial clustering of autism, autoimmunity, and infections, as well as genetic correlations between autism and aspects of immune function. Given this literature, there is an apparent risk of confounding of the reported associations between inflammatory exposures and autism by familial genetic factors in both clinical and epidemiological cohort studies. We highlight recent studies that have attempted to address potential confounding to assess evidence of causal effects of inflammation during early life in autism.

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5. Grineski SE, Ramos K, Renteria R, Collins TW, VanDerslice J, Bilder D, Bakian A. Multigenerational exposures to polluting industries and developmental disabilities. Sci Total Environ;2025 (Jun 13);989:179888.

Animal models suggest that environmental exposures can impact future generations of offspring. Yet, there are limited human epidemiological studies of multigenerational environmental exposures, and even fewer such studies of maternal and paternal exposures. Leveraging a unique data resource in Utah (USA), we examine if offspring (F2, n = 6380) are at increased risk of intellectual disability (ID) if the mother or father (F1) were exposed to polluting industrial facilities while their own mothers (F0) were pregnant. We obtained historical data on polluting industry locations and calculated facility densities within 3 km and 5 km of each child’s (F2) grandmothers’ (F0) residential addresses at time of their mothers’ and fathers’ (F1) births as well as their mother’s address at the time of their birth. We weighted those counts by pairing industry codes with national Risk-Screening Environmental Indicators health risk scores. One standard deviation (SD) increase in the density of facilities near the pregnant maternal grandmother was associated with 1.12 (1.03-1.22) and 1.09 (1.003-1.19) times greater odds of ID at 3 km and 5 km, respectively. Weighing these facility densities by risk, odds ratios associated with SD increases were 1.12 (1.04-1.20, 3 km) and 1.08 (1.003-1.17, 5 km). Associations with facility densities near the pregnant paternal grandmother were positive but weak. Associations with risk-weighted facility density near the pregnant paternal grandmother were stronger at 5 km (1.12, 1.02-1.22) than at 3 km. Results indicated that ancestral exposures, particularly when the maternal grandmother (F0) was pregnant with the mother (F1), may increase risks of developmental disabilities in the next generation (F2).

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6. Hill J, Williams B, McKeown G, Gomersall SR. Description and Evaluation of a Co-design Process Involved in the Creation of a Workforce Training Package Aiding Sport and Exercise Professionals Work with Autistic Young People. J Autism Dev Disord;2025 (Jun 14)

Increasingly, researchers are encouraged to include consumers and stakeholders in the development of health and service provider education. This is particularly important for education relating to autistic people to ensure that resources are developed from a neurodiversity-affirming lens. Limited literature exists outlining or evaluating the processes used within co-design autism research. This study aimed to describe and qualitatively evaluate the co-design process used in the development of a training package for community sport and exercise professionals working with autistic young people. Semi-structured interviews were conducted with the 10 consumers and stakeholders involved in this co-design project. Interviews were analysed using inductive thematic analysis. From the transcripts, four themes emerged. In theme 1 members described characteristics relating to the co-design process they perceived enhanced their engagement. Members emphasised the importance of the project being consumer and stakeholder led, and flexible to support each person’s needs. In theme 2 members described the connection they felt to the other group members, facilitated by the creation of an emotionally safe environment. In theme 3 members discussed how the processes put in place and the supportive environment created resulted in a holistic understanding of the skills and knowledge community sport and exercise professionals need to effectively work with young autistic people. In theme 4 members provided recommendations for future co-design research. Consumer and stakeholders involved in this project described an overall positive experience of the co-design process, with findings resulting in three key recommendations to support future autism co-design research.

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7. Jia X, Gao S, Liu X, Feng Z, Wang X, Lan K, Lu Y, Han L, Wei YB, Liu JJ. Alterations of the endocannabinoid system in autism spectrum disorder: a systematic review and meta-analysis. Eur Arch Psychiatry Clin Neurosci;2025 (Jun 15)

Dysregulation of the endocannabinoid system (ECS) might be related to autism spectrum disorder (ASD). This study conducts a meta-analysis on the dysregulation of the ECS across ASD animal models and individuals with ASD and systematically reviews the impact of these alterations in ASD animal models. Out of 47 papers assessed for eligibility, 16 animal studies and five human studies were included for narrative synthesis and seven and three for quantitative analysis, respectively. The results revealed a significant decrease in hippocampus anandamide (AEA) levels (SMD = -1.06, 95% CI [-1.78, -0.33], p < 0.01) among ASD animal models and a decrease in blood AEA levels in individuals with ASD (SMD = -0.79, 95% CI [-1.28, -0.30], p = 0.002) compared to normal controls. In the prefrontal cortex, 2-arachidonoylglycerol (2-AG) levels were significantly decreased, despite high heterogeneity between studies (SMD = -1.00, 95% CI [-1.93, -0.06], p = 0.04). No significant changes compared to normal controls were observed in levels of AEA (SMD = -0.48, 95% CI [-1.20, 0.25], p = 0.20), 2-AG (SMD = -0.62, 95% CI [-1.27, 0.02], p = 0.06) in combined brain regions. The narrative synthesis revealed that elevated AEA and 2-AG levels could ameliorate core and associated autistic-like symptoms with region and sex-dependent variations in ASD animal models. Future research should focus on specific mechanisms of endocannabinoids regional effects while considering sex-related influences.

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8. Mukherjee SS, Halder A, Singhi AK, Sivakumar K. 2: 1 AV block post ASD device closure – What is the mechanism?. Indian Pacing Electrophysiol J;2025 (Jun 12)

We report a case of atrioventricular (AV) block post successful percutaneous atrial septal defect (ASD) device closure. He had minimal fatigue and presented for his routine follow-up after intervention. His ECG showed 2:1 AV block. The interesting finding was appearance of varying PR interval in the conducted beats evoking possibility of complete heart block (CHB). We review the literature and conclude that changing PR is part of compensation to maintain R-R interval in a typical Wenckebach phenomenon.

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9. Özel F, White RA, Clark KD, Indremo M, Zejlon I, Rüegg J, Papadopoulos FC. Associations between autism, gender dysphoria and gender incongruence: insights from the Swedish Gender Dysphoria Study (SKDS). Psychiatry Res;2025 (Jun 9);351:116591.

BACKGROUND: A higher prevalence of autism spectrum disorder (ASD) and autistic traits among transgender and gender diverse individuals compared to the general population has been reported. However, inconsistent findings and methodological limitations have been noted in the literature. This study aims to investigate the prevalence of ASD diagnoses and autistic traits among individuals with gender dysphoria compared to a cisgender group and to explore associations between autism and self-reported levels of gender incongruence in individuals with gender dysphoria. METHODS: This study is part of the Swedish Gender Dysphoria Study. ASD diagnoses were retrieved from the national patient registers. Autistic traits were assessed using the Ritvo Autism and Asperger Diagnostic Scale-14 (RAADS-14) and Autism Spectrum Quotient (AQ). Gender incongruence was evaluated with the Transgender Congruence Scale. Associations with gender incongruence were examined with linear regression analysis. RESULTS: Participants with gender dysphoria, regardless of birth-assigned sex, had a higher prevalence of ASD compared with cisgender participants (RR = 7.8; 95 % CI = 3.9, 15.3). The gender dysphoria group also scored higher on both the RAADS-14 (MD = 8.0; 95 % CI = 6.6, 9.6) and AQ (MD = 5.3; 95 % CI = 4.0, 6.6). When stratified by birth-assigned sex, the prevalence of ASD did not differ among participants with gender dysphoria. No association was found between ASD and gender incongruence among individuals with gender dysphoria. CONCLUSIONS: Our findings confirm the high co-occurrence of ASD and gender dysphoria and suggest no difference in gender incongruence between autistic and non-autistic people with gender dysphoria.

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10. Surgent O, Andrews DS, Lee JK, Boyle J, Dakopolos A, Miller M, Ozonoff S, Rogers SJ, Solomon M, Amaral DG, Nordahl CW. Sex Differences in the Striatal Contributions to Longitudinal Fine Motor Development in Autistic Children. Biol Psychiatry;2025 (Jun 15);97(12):1150-1162.

BACKGROUND: Fine motor challenges are prevalent in autistic populations. However, little is known about their neurobiological underpinnings or how their related neural mechanisms are influenced by sex. The dorsal striatum, which comprises the caudate nucleus and putamen, is associated with motor learning and control and may hold critical information. We investigated how autism diagnosis and sex assigned at birth influence associations between the dorsal striatum and fine motor development in autistic and nonautistic children. METHODS: We used multimodal assessment of striatal structures (volume and corticostriatal white matter microstructure) and longitudinal assessment of fine motor skills, first at approximately 3 years of age (time 1) and again 2 to 3 years later (follow-up). Fine motor and magnetic resonance imaging (T1 and diffusion) data were collected at time 1 from 356 children (234 autistic; 128 girls) and at follow-up from 195 children (113 autistic; 76 girls). RESULTS: At time 1, associations among fine motor skills, putamen volume, and sensorimotor-striatal fractional anisotropy (sensorimotor-affiliated dorsal striatal structures) were different in autistic boys compared with autistic girls and were not significant for nonautistic children. Further, time 1 sensorimotor-striatal and prefrontal-striatal microstructure predicted fine motor development for autistic girls but not boys. CONCLUSIONS: Sensorimotor-affiliated dorsal striatum structures may contribute to concurrent motor ability and predict fine motor improvement during critical windows of development in a sex-specific and diagnosis-dependent way. Moreover, the dorsal striatum may play a key role in the distinct neural mechanisms underlying motor challenges in autistic boys and girls.

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11. Tamaoki Y, Kroon SL, Williams BM, Riley JR, Engineer CT. Early neural dysfunction reflected in degraded auditory cortex responses in pre-regression heterozygous Mecp2 rats. Neurobiol Dis;2025 (Jun 15);210:106926.

Rett syndrome, a genetic disorder caused by mutations in the X-linked Mecp2 gene, is characterized by typical early development followed by rapid developmental regression between 6 and 18 months of age. Affected individuals exhibit seizures, cognitive impairments, motor deficits, and difficulties in speech-language processing. Post-regression rodent models of Rett syndrome have been observed to follow similar regression, presenting sensory processing difficulties during auditory discrimination tasks, as well as degraded auditory cortical responses. However, little is known about the auditory processing prior to the onset of regression symptoms. This study documents primary auditory cortex responses to sounds in pre-regression heterozygous Mecp2 rats compared to age-matched wild-type controls. Pre-regression Mecp2 rats exhibited weaker and delayed cortical responses to speech sounds, alterations in the temporal processing of rapidly presented sounds, and an overrepresentation of high-frequency tones in conjunction with a reduction in the cortical representation of low-frequency tones. Despite these impairments, pre-regression Mecp2 rats demonstrated intact neural classifier performance for consonant discrimination, which is consistent with the high accuracy these pre-regression Mecp2 rats exhibit for a behavioral consonant discrimination task. These findings reveal that cortical deficits in Mecp2 rats emerge before behavioral regression. Insights derived from this study expand upon the current understanding of the progression of sensory processing deficits in Rett syndrome and other neurodevelopmental disorders and lay the groundwork for the development of therapeutics for this population.

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12. Xiang AH, Lin JC, Chow T, Yu X, Martinez MP, Chen Z, Eckel SP, Schwartz J, Lurmann FW, Kleeman MJ, McConnell R, Rahman MM. Discordant sibling analysis of autism risk associated with prenatal exposure to tailpipe and non-tailpipe particulate matter pollution. Environ Res;2025 (Jun 15);275:121449.

BACKGROUND: We previously assessed associations of prenatal exposure to fine particulate matter (PM(2.5)) tracers reflecting tailpipe (elemental carbon [EC] and organic carbon [OC]) and non-tailpipe emissions (copper [Cu], iron [Fe] and manganese [Mn]) with risk of autism spectrum disorder (ASD) in a large pregnancy cohort. To address genetic and family environment confounding, we conducted an ASD-discordant sibling study. METHODS: Data included 4024 children (1837 with and 2187 siblings without ASD) born to 1801 unique mothers who had at least one child diagnosed with ASD by age 5, and one child without ASD. Prenatal exposures to total PM(2.5), trace elements Cu, Fe, Mn, EC, and OC and dispersion-modeled near-roadway-air-pollution (NRAP) from freeway and non-freeway source were obtained using maternal addresses during pregnancy. Conditional logistic regression was used to assess ASD risk associated with exposures adjusting for covariates. Results were reported as odds ratio (OR, 95 % CI) per inter-quartile increment of each exposure. RESULTS: In single-pollutant models, child ASD risk (OR; 95 % CI) was associated with gestational exposures to non-tailpipe source Cu (1.17; 1.03-1.33), Fe (1.26; 1.07-1.48), Mn (1.29; 1.11-1.50); but not likewise associated with tailpipe source EC (1.10; 0.92-1.32) and OC (1.10; 0.91-1.32). Total PM(2.5) and non-freeway NRAP were both associated with ASD risk. Adjusting for total PM(2.5) or NRAP attenuated the ASD associations with Cu, Fe, and Mn but they remained largely statistically significant. By trimester analysis showed the associations with Cu, Fe, and Mn were significant in the first two trimesters. CONCLUSION: This ASD-discordant sibling study confirmed previously reported ASD risk associated with prenatal exposure to PM(2.5), NRAP and non-tailpipe particulate trace-element Cu, Fe, and Mn, particularly in the first two trimesters, thus, increasing evidence of causality.

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13. Xiao J, Ming Y, Li L, Huang X, Zhou Y, Ou J, Kou J, Feng R, Ma R, Zheng Q, Shan X, Meng Y, Liao W, Zhang Y, Wang T, Kuang Y, Cao J, Li S, Lai H, Chen J, Wang Q, Dong X, Kang X, Chen H, Menon V, Duan X. Personalized Theta Burst Stimulation Enhances Social Skills in Young Minimally Verbal Children With Autism: A Double-Blind Randomized Controlled Trial. Biol Psychiatry;2025 (Jun 15);97(12):1139-1149.

BACKGROUND: Minimally verbal children with autism are understudied and lack effective treatment options. Personalized continuous theta burst stimulation (cTBS) targeting the amygdala and its circuitry may be a potential therapeutic approach for this population. METHODS: In a double-blind randomized controlled trial, minimally verbal children with autism (ages 2-8 years) received 4 weeks of cTBS. An amygdala-optimized functional connectivity (AOFC) group (n = 23) received personalized stimulation targeting a left dorsolateral prefrontal cortex site functionally connected with the amygdala. A non-optimized (NO) control group (n = 21) received stimulation at a standard prefrontal site. We assessed changes in Autism Diagnostic Observation Schedule scores, amygdala volume, spontaneous neural activity, and FC. RESULTS: Personalized AOFC-guided cTBS improved social and communication skills with an effect size twice that of the NO group (Cohen’s d = 0.55 vs. 0.24). The AOFC group showed greater reductions in amygdala volume, spontaneous neural activity, and hyperconnectivity. Network-level amygdala connectivity changes with default mode, frontoparietal, and dorsal attention networks were correlated with clinical improvements. Field mapping analysis revealed that greater electric field overlap between standard and optimized targets predicted better treatment outcomes. CONCLUSIONS: Personalized AOFC-guided cTBS enhanced social skills and communication in minimally verbal children with autism by modulating amygdala structure and connectivity. Changes in amygdala network connectivity predicted clinical improvements, suggesting a mechanistic link between neural circuit plasticity and behavioral outcomes. These findings demonstrate the potential of precision-targeted neuromodulation in addressing a critical gap in autism treatment for this understudied population.

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14. Yu Z, Luo Z, Zheng J, Lu L, Tang C, Qu C. Autism spectrum disorders and the volume of the striatum and Amygdala: A Mendelian randomization study. Brain Res;2025 (Jun 12):149781.

BACKGROUNDS/AIMS: A number of studies have documented alterations in the structure and function of the striatum in individuals diagnosed with autism spectrum disorder (ASD). Nevertheless, the precise genetic mechanisms underpinning the relationship between autism spectrum disorder (ASD) and striatum and amygdala volume remain to be elucidated. The objective of this study was to estimate the causal effect of ASD on striatum and amygdala volume. METHODS: Summarized data of genome-wide association studies (GWAS) were separately downloaded from the IEU (Integrative Epidemiology Unit) open GWAS project (22138 participants of Europeans (100%), 18,382 cases of ASD and 27,969 controls, with a total of 33,219 brain imaged samples), the Enhancing Neuroimaging Genetics through Meta-Analysis Consortium (ENIGMA) (15640 participants of Europeans (96.5%) and non-Europeans). The MR-egger intercept test, MR-presso and Cochran’s Q statistic was used to examine the pleiotropy and heterogeneity, respectively. MR-egger, weighted median, inverse variance weighted, simple mode, and weighted mode methods were used to evaluate the causal association between striatum and amygdala volume and ASD. Finally, the effect of a single SNP (single nucleotide polymorphism) was used to test the SNP bias. RESULTS: The increased change rate of the putamen shows a strong and statistically significant association with ASD risk (P(IVW) = 0.015, P(FDR) = 0.044), with a large beta value (β(SE) = 8.272(3.401), 95 %CI: 1.605 to 14.939) indicating a substantial effect size. This makes it a potentially important changes caused by ASD. However, the increased change rate of the amygdala shows a positive but not statistically significant association with ASD risk (P(IVW) = 0.119, P(FDR) = 0.593). The beta value (2.527) is smaller, and the confidence interval includes zero, suggesting that this result is not reliable as a predictor of ASD risk. The other part of GM (grey matter) of striatum and amygdala volume also showed unsignificant result due to small beta values or unsignificant FDR p values. CONCLUSIONS: The putamen’s change rate appears to be a significant change caused by ASD which may be a strong predictive capability for ASD risk, while the amygdala’s change rate and GM of striatum and amygdala volume does not show a significant predictive capability in this context. The present study provides evidence of a genetic relationship between ASD and putamen volume. Further investigation is required to elucidate the mechanisms underlying the genetic effect of changes in putamen structure and function on ASD.

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15. Zhang J, Yuan M, Liu Y, Zhong X, Wu J, Chen W. Bisphenol A exposure and neurodevelopmental disorders and problems in children under 12 years of age: A systematic review and meta-analysis. J Hazard Mater;2025 (Jun 15);490:137731.

BACKGROUND: Bisphenol A (BPA) exposure may lead to neurodevelopmental disorders and problems (NDPs) in children under 12 years old. In recent years, the number of relevant studies has increased, but the evidence is inconsistent. Therefore, we conducted a comprehensive systematic review and meta-analysis to determine the association between BPA exposure and NDPs and potential gender differences. METHODS: A literature search was conducted in eight bibliographic databases for peer-reviewed research articles published from database inception to October 11, 2024. Eligible studies were epidemiological, observational studies in children under 12 years old, which evaluated the associations between BPA of biosamples and NDPs. The converted effect sizes were synthesized using multilevel random effects meta-analysis models. Meta-regression analysis, sensitivity analysis, unmeasured confounding bias, and publication bias tests were examined to substantiate the results. RESULTS: The search identified 1090 unique studies, 32 of which involving 15,669 participants were finally included in the meta-analysis. The meta-analysis showed that BPA exposure was associated with intellectual disability (Cohen’s d = 0.14, 95 %CI = 0.06-0.22), autism spectrum disorder (ASD, Cohen’s d = 0.10, 95 %CI = 0.02-0.17), attention deficit and hyperactivity disorder (ADHD, Cohen’s d = 0.28, 95 %CI = 0.10-0.47), and communication disorders (Cohen’s d = 0.12, 95 %CI = 0.01-0.23) in all children. Gender differences exist while BPA was associated with intellectual disability, ASD, ADHD, and motor disorders in boys, and with intellectual disability and ADHD in girls. CONCLUSION: This study indicated that BPA exposure was associated with an increased risk of NDPs in children, particularly in boys, underscoring the importance of considering BPA exposure as a potential risk factor for children’s brain health.

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16. Zhang Y, Li F, Wu H, Du W, Shu J, Wang A, Xu C, Li C, Wang Y, Hu S. Genetic neurocognitive profile of autism unveiled with gene transcription. Neurobiol Dis;2025 (Jun 15);210:106925.

How neurocognitive processes elaborate phenotypic heterogeneity within autism spectrum disorder (ASD) remains unknown. Applying the principal component analysis to the Neurosynth database, we established neurocognitive profiles to characterize the phenotypic heterogeneity of ASD, revealing a cortical hierarchical axis that separates the temporal cortex from other networks. By integrating neurocognitive profiles with transcriptomic data, we found that gene sets shaping the patterns of neurocognitive profiles are enriched in ASD-related biological processes and ASD pathogenic risk. Using a data-driven approach, we identified a topographic network for ASD, comprising the temporal, frontal, somatosensory, and visual cortices, with its transcriptomic signatures differentiating between regions over neurodevelopment. Additionally, functional reorganization in ASD within the topographic network has occurred with the temporal cortex as the central node. Collectively, our results reveal spatially covarying transcriptomic and neurocognitive profiles, emphasizing the influence of functional reorganization and its underlying genetic mechanism on phenotypic heterogeneity in ASD.

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