1. Ahmed A, Rasheva V, Bae M, Murari K, Cheng N. Electroencephalography signals in a female Fragile X Syndrome mouse model. Neuroimage. 2026: 121866.

BACKGROUND: Fragile X syndrome (FXS) is the leading monogenic cause of Autism. No broadly effective support option currently exists for FXS, and drug development has suffered many failures in clinical trials based on promising preclinical findings. Thus, effective translational biomarkers of treatment outcomes are needed. Recently, electroencephalography (EEG) has been proposed as a translational biomarker in FXS. Recent years have seen an exciting emergence of novel EEG signal analyses from FXS patients. However, there is a notable gap in corresponding analyses conducted on animal models of the disorder. Being X-linked, FXS is more prevalent in males than females, and there exist significant phenotype differences between males and females with FXS. Recent studies involving male FXS participants and rodent models have identified an increase in absolute gamma EEG power, while alpha power is found to be either decreased or unchanged. However, there is not enough research on female FXS patients or models. In addition, studying EEG activity in both young and adult FXS patients or rodent models is crucial for better understanding of the disorder’s effects on brain development. Therefore, using the well-established fmr1 knockout (KO) mouse model of FXS, we aim to compare EEG signal between female wild-type (WT) and female model mice at both juvenile and adult ages. METHODS: Frontal-parietal differential EEG was recorded using a stand-alone Open-Source Electrophysiology Recording system for Rodents (OSERR). EEG activity was recorded in three different conditions: a) in the subject’s home cage, and in the arenas for b) light-dark test and c) open field test. Absolute and relative EEG power as well as peak alpha frequency, theta-beta ratio, phase-amplitude and amplitude-amplitude coupling, and EEG signal complexity were computed for each condition. Analyses of absolute and relative power, particularly gamma power, were a priori confirmatory based on established findings in human and rodent FXS literature. All additional EEG features (peak alpha frequency, theta-beta ratio, cross-frequency coupling, and signal complexity) were treated as exploratory. RESULTS: In our study, we found EEG signals were stable across different recording conditions. Our results indicate that absolute alpha, beta, gamma and total EEG power is increased in the female model compared to WT controls, and the difference is more pronounced at the adult age. Alongside, relative theta power is decreased in the model. Additionally, phase-amplitude and amplitude-amplitude coupling are altered in the model. Furthermore, peak alpha frequency is increased, and theta-beta ratio is decreased in the model. Lastly, no change in EEG signal complexity is found. DISCUSSION AND CONCLUSION: Consistent with most findings from FXS patients and rodent models, our results demonstrated an increase in gamma power in fmr1KO female mice, reinforcing gamma power as a robust and reliable EEG phenotype across FXS models. Additionally, theta-gamma cross frequency amplitude coupling is inversely coupled in female FXS model, which is similar to what has been reported in FXS patients. Overall, our findings reveal that some, but not all EEG biomarkers observed in FXS patients are replicated in the female FXS model. For example, amplitude-amplitude coupling exhibited a similar trend between the fmr1KO mouse models and FXS patients, supporting its potential as a translational EEG biomarker. In contrast, other measures such as peak alpha frequency, theta-beta ratio, and brain signal complexity showed notable discrepancies between the mouse models and human data. Additionally, when compared to previously reported EEG changes in male FXS mouse models, our results highlight the presence of a potential sex-based difference in EEG phenotypes at both juvenile and adult stages of fmr1KO mouse models. Together, our study indicates that certain EEG parameters may be more translatable between rodent models and FXS patients than others and underscore the importance of considering sex and developmental stage as a critical factor when using EEG as a biomarker in FXS research.

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2. Akbuga E. Preliminary evidence for backward walking to reduce toe walking in autism spectrum disorder: A single-case experimental pilot study. Acta Psychol (Amst). 2026; 265: 106707.

This pilot study investigated whether backward walking (BW) exercises could reduce toe walking behaviors (TWB) in a child with autism spectrum disorder (ASD) and evaluated the utility of pedobarographic measurements to quantify TWB. This prospective single-case pilot study, conducted per SCRIBE guidelines, employed an A-B-A reversal design with 1-week baseline, 9-week intervention, and 1-week monitoring phases. The participant was a 41-month-old girl with ASD who exhibited TWB (pseudonym « Daisy »), and the BTS P-Walk platform was used to measure plantar surface area. Backward walking exercises were implemented on a treadmill five days per week, adapted to developmental characteristics. Data analysis included visual analysis, internal and social validity, and effect size calculations. Results showed gradual increases in plantar surface area bilaterally, suggesting a potential reduction in TWB. Preliminary findings indicated improvements for the right foot during weeks 8-9 (x̄ =42.78-42.82 cm(2) vs. baseline x̄ =33.58 cm(2); p = 0.009, Tau = 1, IRD = 1) the left foot (x̄ =45.22-47.28 cm(2); p ≤ 0.016, Tau≥0.92, IRD ≥ 0.80), with these statistics providing supportive evidence for the observed changes. The monitoring phase indicated that improvements were maintained, albeit attenuated. Pedobarographic measurements may provide a quantitative assessment of TWB. BW exercises appeared to reduce TWB and may benefit motor development in this case. The preliminary findings derived from the single-case design limit generalizability; therefore, larger samples should be tested before making clinical recommendations. Future research should include controlled studies and examine the biomechanical analyses and muscle properties underlying the mechanisms of BW.

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3. Deng X, Li B, Tang J, Yu B, Chen R, Guo T. The association of birth weight with children’s anxiety, depression and developmental disabilities. Early Hum Dev. 2026; 218: 106537.

BACKGROUND: Low birth weight (LBW) has been linked to the risk of developmental disabilities. However, few studies have been large enough to assess the associations between children’s mental health (anxiety, depression) and a comprehensive range of developmental disabilities in a large general children’s population, and limited studies have examined dose-response associations. METHODS: This population-based, nationally representative cross-sectional study included 35,379 children aged 6-17 years who participated in the 2022-2023 National Survey of Children’s Health (NSCH) in the U.S from July 2022 to January 2024. Data of NSCH survey were based on retrospective parental or primary caregiver self-reports. Multivariable-adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by multivariable logistic regression models to explore the association between low or high birth weight, anxiety, depression, behavior problems, developmental delay, intellectual disability, speech disorder, learning disability, autism spectrum disorder (ASD), and attention deficit disorder/attention-deficit hyperactivity disorder (ADD/ADHD). RESULTS: The weighted prevalence for each of the adverse outcomes was as follows: anxiety, 10.6; depression, 5.0; behavior problems, 7.6; developmental delay, 5.3; intellectual disability, 0.8; speech disorder, 6.5; learning disability, 6.6; ASD, 3.2; and ADD/ADHD, 10.5. The prevalence of LBW was 9.5 (95%CI, 8.9-10.2, [weighted]). LBW was associated with a higher risk of anxiety (OR, 1.14 [95% CI, 1.02-1.27]), behavior problems (OR, 1.29 [95% CI, 1.14-1.47]), developmental delay (OR, 2.18 [95% CI, 1.91-2.48]), intellectual disability (OR, 2.00 [95% CI, 1.45-2.75]), speech disorder (OR, 1.61 [95% CI, 1.42-1.84]), learning disability (OR, 1.69 [95% CI, 1.49-1.92]), ASD (OR, 1.32 [95% CI, 1.09-1.59]) and ADD/ADHD (OR, 1.36 [95% CI, 1.22-1.52]), respectively. There was no statistically significant association between high birth weight and anxiety, depression, or any developmental disabilities. The dose-response analysis showed a decreasing association between increasing birth weight and anxiety, behavior problems, developmental delay, intellectual disability, speech disorder, learning disability, ASD, and ADD/ADHD, respectively. Similar results were obtained in the sensitivity analyses. Compared to youth without LBW and PTB, youth with LBW and PTB have the highest risk of outcomes. CONCLUSION: In conclusion, this large population-based, nationally representative, comprehensive study demonstrates that LBW was associated with a higher risk of anxiety and developmental disabilities in US youths aged 6-17 years. Our findings suggested that for monitoring, maintaining, and supporting the health of children born with LBW.

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4. Doyumğaç İ, Söner O, Arslan G. Autism, Belief, and Society: Voices of Families in Cultural and Religious Contexts. J Autism Dev Disord. 2026.

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5. Harripaul R, Rabia A, Vasli N, Mikhailov A, Rodrigues A, Pastore SF, Muhammad T, Madanagopal TT, Hashmi AN, Tran C, Stan C, Aw K, Zai CC, Azam M, Mahmood S, Heidari A, Qamar R, French L, Tripathy S, Agha Z, Iqbal M, Ghadami M, Santangelo SL, Bozorgmehr B, Al Ayadhi L, Sasanfar R, Maqbool S, Hassan A, Knowles JA, Ayub M, Vincent JB. Autism spectrum disorder trios from consanguineous populations are enriched for rare homozygous variants, identifying 32 new candidate genes. Sci Rep. 2026.

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6. Li Z, Wang J, Feng T, Lu W. Alpha-lipoic acid attenuates valproic acid-induced autism-like phenotypes in zebrafish by enhancing antioxidant capacity and repressing oxidative stress, inflammation, apoptosis, and HPI-axis signaling. Comp Biochem Physiol C Toxicol Pharmacol. 2026: 110518.

Autism spectrum disorder (ASD) is a complex neurodevelopmental condition with identified etiological mechanisms, yet effective treatments remain elusive. Individuals with ASD often exhibit compromised antioxidant defenses and are subject to oxidative stress. In this study, we used an established zebrafish (Danio rerio) model of autism with valproic acid (VPA) and subsequently administered 20 μg/mL Alpha-lipoic acid (ALA) to assess its effects on oxidative stress markers, transcriptional alterations in genes associated with autism, inflammatory mediators, apoptosis, the hypothalamic-pituitary-interrenal (HPI) axis, and aggressive behavior. Our results demonstrated that ALA treatment significantly enhanced the activity of antioxidant enzymes, particularly glutathione S-transferase (GST) and glutathione peroxidase (GPX), while increasing glutathione (GSH) levels and reducing malondialdehyde (MDA) concentrations. ALA treatment resulted in lower expression levels of inflammatory cytokines TNF-α and IL-6 mRNA. ALA downregulated the expression of apoptotic markers such as caspase-3, caspase-8, and caspase-9, as well as decrease the number of apoptotic cells. Additionally, behavioral assessments indicated a restoration of aggressive behavior, alongside a reduction in the expression of HPI axis-related hormones, including CRHα, CRHβ, UI, GR and MR, leading to decreased systemic cortisol level. Furthermore, ALA treatment reduced the expression of autism-related genes like shank3a, chd8, adsl, and mbd5. Molecular docking analyses suggest ALA may directly interact with proteins from these genes, offering new insights into its role in autism-related pathways. Collectively, our findings suggest that ALA may mitigate VPA-induced ASD-like symptoms by enhancing antioxidant capacity, alleviating oxidative stress, modulating inflammatory responses, and repressing apoptotic and HPI axis activity, thereby offering a potential therapeutic avenue for the management of ASD symptoms.

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7. Smith PH, Ventimiglia J, Wright J, Rast JE, Schendel DE, Mullachery PH, Lee BK, Shea LL. Brief Report: Healthcare Utilization and Expenditure Trends Among Autistic Transition Age Youth. J Autism Dev Disord. 2026.

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8. Song Y, Guo J, Yang F, Wu Y, Zhang P, Chen Q. Effects of fine motor-skill oriented sports games on core symptoms in children with autism: a randomized controlled trial. Trials. 2026.

AIMS: Based on the observed correlation between core symptoms and fine motor function in children with ASD, this study aimed to evaluate the therapeutic effect of a novel, fine motor task-oriented sports game intervention, compared to traditional SI. METHODS: Forty-five children with ASD were randomly allocated to two groups. The experimental group received the fine motor-oriented sports game intervention, while the control group received traditional SI. Core symptoms and fine motor function were assessed using the ABC, CABS, CARS, and PDMS-FM scales at both baseline and post-intervention, with the ABC scale serving as the primary outcome measure. RESULTS: In the randomized comparison, the experimental group showed superior outcomes to the control group post-intervention, with significantly greater reductions in ABC, CARS, and CABS scores and a greater increase in PDMS-FM score (all P < 0.05). CONCLUSIONS: The fine motor-oriented sports game intervention proved more effective than SI in ameliorating the core symptoms and improving fine motor function in children with ASD. TRIAL REGISTRATION: The study has been registered at ChiCTR.org (ChiCTR2400086052) on 2024-06-24.

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9. Tafla TL, Rasia Lira P, Brandi Gomes Godoy P, Shephard E. Conducting Meaningful Participatory Autism Research in Latin America: An Example of Contextual Challenges Identified and Lessons Learned from the Indigenous Support Network In Brazil. Autism. 2026: 13623613261434813.

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10. VanDaalen RA, Zhao JL, Hsiao YJE, Karsting H, Cai RY, Kim JP, Fung LK. Correction: Exploring Correlations of Unemployment, Underemployment, and Well-Being Among Autistic Job Seekers by Race in the United States. J Autism Dev Disord. 2026.

PURPOSE: Autistic adults have high levels of unemployment and underemployment, which may have detrimental effects on their financial and psychological well-being. In the current project, we explore correlates of psychological and financial well-being, as well as depressive symptoms, with different levels of employment while examining whether race moderates these relationships. METHODS: We utilized survey data from autistic job seekers in the United States who expressed interest in a larger clinical trial of a supported employment program. RESULTS: Among the 710 participants, 248 (34.9%) were currently employed; among the employed participants, 127 (51.2%) met at least one criterion for underemployment. In general, there were no significant differences by employment status in depressive symptoms, psychological well-being, or financial well-being. However, when controlling for age, gender, and education level, race/ethnicity significantly moderated the relationship between employment status and depressive symptoms. Specifically, fully employed Asian American participants had significantly fewer depressive symptoms compared to their underemployed counterparts. CONCLUSION: The present study highlights the nuances of employment status and well-being among diverse autistic individuals, especially Asian American autistic individuals.

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