1. Brennan E, Lampinen LA, Paek H, Wang X, Romano H, Bal VH. Deconstructing Information About Autism Diagnosis in Adults on TikTok: A Cross-Sectional, Descriptive Content Analysis. J Autism Dev Disord. 2025.

PURPOSE: Social media has increasingly become a platform where individuals share and seek information about autism. However, recent research indicates that autism-related content on TikTok often contains misleading or inaccurate information. Additionally, the number of adults seeking first-time autism diagnoses has increased over the past several years, potentially due to increased public awareness and exposure to content on social media. In order to understand how autistic adults are engaging with TikTok, there is a need to examine content focused specifically on autism in adulthood. This study aimed to address this gap by analyzing TikTok content associated with the hashtags #actuallyautistic, #latediagnosedautistic, and #autism. METHODS: A content analysis of 150 videos examined themes, attitudes, clinical accuracy, and user engagement metrics. Additional analyses were run to examine common traits that users reported in relation to autism. RESULTS: A significant portion of videos were either personal in nature or misleading. Content analysis showed that many topics centered around identity related to autism diagnosis, and many associated themes were negative. There were significant differences in content between hashtags, indicating potential biases within various channels of information. CONCLUSION: The broad reach of these videos indicates that TikTok is a potent platform for autism awareness, education, and identity exploration. This research underscores the role of social media in shaping public perception of autism and highlights the need for enhanced digital literacy to navigate and disseminate information. It also provides insight into discussions of autistic identity, which may help providers connect more effectively with this growing population.

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2. Brothwell J, Jeje O, Mashamaite D, Fanucchi S. Novel interactions between FOXP2 and PAX6: Implications for neural development and autism spectrum disorders. Biochim Biophys Acta Proteins Proteom. 2025; 1874(1): 141110.

FOXP2 and PAX6 are transcription factors essential for neural development, with mutations in both linked to autism spectrum disorders (ASDs). Their DNA-binding domains include a forkhead domain (FHD) for FOXP2 and a paired domain (PD) plus homeodomain (HD) for PAX6. We investigated whether the FOXP2 FHD interacts directly with PAX6 PD or HD, and how such interactions influence DNA binding. Fluorescence anisotropy showed that all three domains bind specifically to their respective DNA targets with similar affinities. The FOXP2 FHD also interacts directly with both PAX6 PD and HD, with low micromolar binding affinities. Despite its stronger intrinsic DNA affinity, the FHD was displaced from its target DNA by both PAX6 domains, suggesting that protein-protein interactions can override DNA affinity under competitive conditions. In contrast, FOXP2 could not displace PD or HD from their DNA targets. Molecular docking supported these findings: DNA-protein interfaces were largely unchanged by the second protein, but protein-protein interfaces were strongly influenced by DNA occupancy. The H3 helix of FHD was identified as a central point for assembly, contributing to both DNA and protein interfaces. When FHD was bound to DNA, H3 was occupied, forcing PD or HD to dock at alternative, less optimal sites. HD maintained stronger contacts in these rearranged states, consistent with its greater competitive strength. This asymmetric interplay indicates competitive dominance by PAX6 and suggests mechanisms that could underlie transcriptional regulation in neurodevelopment.

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3. Cacciato-Salcedo S, Lao-Rodríguez AB, Malmierca MS. Sex- and age-specific effects on auditory brainstem responses in the valproic acid-induced rat model of autism. Hear Res. 2025; 468: 109470.

Prenatal exposure to valproic acid (VPA) provides a well-established rodent model of autism, yet its effects on auditory brainstem/midbrain processing across sex and development remain elusive. We recorded click-evoked auditory brainstem responses (ABRs) in Long-Evans rats that received prenatal VPA (400 mg/kg, gestational day 12) and in matched controls at prepubertal (postnatal days 30-45) and adult (65-120) stages under urethane anesthesia. We analyzed peak amplitudes, latencies, inter-peak intervals, and amplitude ratios across sound levels. Auditory thresholds remained comparable among groups. In controls, females showed larger amplitudes for waves I-II, shorter latencies for waves I, II, and IV, and steeper amplitude-intensity slopes for waves II, III, and V than males, indicating stronger level-dependent recruitment. Maturation enhanced early brainstem and midbrain responses by increasing amplitude growth (wave II) and shortening latencies (waves II-V), with effects more pronounced in females. Prenatal VPA exposure reduced wave II amplitude and delayed early peaks (I-III) in females, accompanied by elevated amplitude ratios, whereas in males it mainly affected later responses by reducing amplitudes for waves III-V and prolonging inter-peak latencies (I-III, III-V). These findings show that sex, age, and prenatal VPA exposure distinctly shape auditory brainstem/midbrain function.

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4. Castro K, Riesgo R, Gadia C. Reply to the letter ‘Beyond overdiagnosis: reframing autism prevalence’. J Pediatr (Rio J). 2025; 101(6): 101469.

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5. Dwivedi S, Rajput P, Akhtar A, Goli SH, Dusane A. Preclinical models for autism spectrum disorder: past, present, and future. Neuroscience. 2025; 591: 186-204.

Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders linked to neurobehavioral abnormalities in children. Despite substantial research suggesting the role of environmental and genetic variables in ASD development, the etiology and pathophysiology of autism still need exploration. To unveil the pathophysiology, genetics, and therapeutics of autism, many preclinical animal models are employed, with rodent models being most trusted. In the last two decades’ various non-rodent animal models and in vitro models for autism have been proposed, which are quick, economic, and trustworthy to investigate. However, there are concerns about mimicking behavioral and molecular features of autism. In this review, we have compiled the preclinical models that can help us comprehend the phenotypic and molecular characteristics of autism. The review discusses the reliability of available models along with their advantages and disadvantages. The inference from the review will provide insight to the researchers into all possible preclinical models for autism and select the best one to improve the translational value in ASD research.

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6. G SD, Grosser KF, Cummings KK, Bradley C, Garcia TP, Tapia AL, Pretzel RE, Nadler C, Moody EJ, Barger B, Reyes NM, Fallin MD, Daniels JL. Changes in Autism Traits from Early Childhood To Adolescence in the Study To Explore Early Development. J Autism Dev Disord. 2025.

PURPOSE: The objectives of this study were to investigate associations between co-occurring developmental, psychiatric, behavioral, and medical symptoms and conditions and autism spectrum disorder (ASD) traits, as well as predictors of changes in autistic traits from early childhood to adolescence. METHODS: Participants from the Study to Explore Early Development (SEED) were identified as having autism spectrum disorder (ASD) (n = 707), another developmental disorder (DD) (n = 995), or as a population comparison group (POP) (n = 898). Caregivers completed the Social Responsiveness Scale-2nd edition (SRS-2) to measure autistic traits and were asked about co-occurring symptoms and conditions when their child was 2-5 years old and 12-16 years old. Children completed the Mullen Scales of Early Learning (MSEL) when they were 2-5 years old. RESULTS: Regression models revealed that in early childhood and adolescence, multiple co-occurring symptoms and conditions were significantly associated with higher SRS-2 scores (e.g., motor, sensory, and sleep problems for children with ASD and DD). Within the ASD and DD groups, but not the POP group, lower MSEL scores at childhood were associated with greater increases in SRS-2 scores between early childhood and adolescence. CONCLUSIONS: Findings suggest that motor, sensory, and sleep problems may be important intervention targets for ASD and DD youth with elevated SRS-2 scores and that interventions that target cognitive functioning in childhood may be important to modify trajectories of autistic traits from childhood to adolescence.

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7. Kalinyak A, Simmons GL, Corbett B, Lerner M, White SW. Fear of Negative Evaluation and Social Anxiety in Autism: A Case for Multi-method Assessment. J Autism Dev Disord. 2025.

PURPOSE: Fear of negative evaluation is a diagnostic criterion for social anxiety disorder (SAD). Research demonstrates this may not always occur in autistic individuals who have other markers of SAD. We aimed to characterize fear of negative evaluation in autistic children utilizing a sample of 239 autistic youth ages 10-16. METHODS: Participants completed self-report questionnaires of social anxiety and fear of negative evaluation. They also participated in a conversation task coded by trained observers to measure social anxiety. RESULTS: Although self-reports of social anxiety and fear of negative evaluation were strongly correlated, they did not match in-the-moment coding of social anxiety from trained observers; this may be partially explained by differences between state and trait experience and the conversational environment. Furthermore, greater levels of autistic traits related to higher levels of social anxiety and to fear of negative evaluation. CONCLUSIONS: Fear of negative evaluation, which is the primary cognitive process involved in social anxiety, was strongly associated with social anxiety in this autistic sample of youth.

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8. Ma Y, Bauer HF, Bockmann J, Schön M, Boeckers TM, Lutz AK. Shank3 related oligodendrocyte alterations in autism are restored by Erk pathway inhibition. Mol Psychiatry. 2025.

White matter abnormalities are consistently observed in Shank3-related autism spectrum disorders (ASD), yet the mechanisms underlying oligodendrocyte dysfunction and myelination deficits remain poorly characterized. Here, we demonstrate that Shank3 deficiency disrupts oligodendrocyte development by promoting oligodendrocyte precursor cell (OPC) proliferation while impairing functional maturation and myelination. Mechanistically, Shank3 deficiency induced hyperactivation of the Erk signalling pathway, which compromised oligodendrocyte maturation and contributes to hypomyelination. Pharmacological inhibition of the Erk pathway effectively restored oligodendrocyte maturation in vitro, rescued myelination deficits in vivo, and partially improved autism-related behaviors and motor function in Shank3-deficient mice. Transcriptomic analyses furtherly revealed dysregulation of Wnt signalling, particularly the upregulation of Wnt5a, a key ligand of the non-canonical Wnt pathway, in Shank3-deficient oligodendrocytes. Consistently, Wnt5a treatment was found to activate Erk signalling in primary oligodendrocytes and replicate the observed myelination deficits. These findings uncover the Wnt5a-Erk axis as a critical regulator of oligodendrocyte dysfunction in Shank3-related ASD and highlight its therapeutic potential for addressing associated white matter deficits.

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9. Rabba AS, Lampinen L, Meldrum P, Dwyer P, South M, Taylor L, Uljarevic M, Bal VH. Understanding Barriers to Assessment and Diagnosis of Autism in Adulthood: Where Are We Now and How Do We Move Forward?. Autism Res. 2025.

Assessment and diagnosis of autism in adulthood is a growing area of interest for both clinical and research practice. In this commentary, we present a thematic analysis following the first International Society for Autism Research Special Interest Group (SIG) focused on assessment and diagnosis of autism in adulthood. An increasing recognition of missed or misdiagnosed autistic adults is highlighted throughout the commentary. Recommendations for reducing barriers in diagnostic processes are reviewed, including improving existing adult autism measures and developing new ones, especially self-report/interview tools capturing what cannot be externally observed; providing more information about the process ahead of time and better post-diagnostic support; better assessment of psychosocial and mental health histories; training to promote clinicians’ understanding of adult autism; and the importance of considering culture. Professional and government bodies should support the development of neuroaffirming, client-centered practice guidelines that actively include input and co-design from autistic adults.

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10. Sollis LJ, Wall DP, Washington PY. Compact subsets of autism screening items predict clinical diagnoses with a machine learning analysis of the QCHAT-10. Sci Rep. 2025; 15(1): 39091.

Early identification improves life outcomes for individuals with autism. This study addresses a central question: do compact subsets of the most predictive QCHAT-10 items, when fed into machine learning (ML) models trained to reproduce the full questionnaire’s screening result, generalize to predicting clinician-established autism diagnoses in independent clinical settings? We applied ML to the 10-question QCHAT-10, training models on New Zealand (n = 1054) and Saudi Arabian (n = 506) datasets with QCHAT-derived labels and testing on Polish data with clinical diagnoses (n = 252). Recursive Feature Elimination identified four-item models retaining three common features: eye contact, following gaze direction, and pretend play. When tested on clinically-diagnosed Polish cases at the 0.3 prediction threshold, the New Zealand model achieved an AUROC of 85% ± 13 (sensitivity 91%, specificity 50%), while the Saudi model reached 87% ± 11 (sensitivity 84%, specificity 80%), compared to the Polish four-item model’s cross-validation AUROC of 91% ± 5. These findings demonstrate partial transfer from the prediction of assessment scores to clinical diagnosis. The convergence on eye contact, gaze following, and pretend play suggests these behaviors represent robust autism risk markers. Compact assessment tools offer advantages, including reduced burden, shortened administration, and simplified deployment, with direct applications for targeted digital phenotyping.

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11. Ulaşman S, Sivrikaya T. Digital Social Stories for Teaching Earthquake Safety Skills to Individuals With Autism Spectrum Disorder. J Autism Dev Disord. 2025.

PURPOSE: This study evaluates digital social stories’ effectiveness in helping individuals with autism spectrum disorder acquire, generalize, and maintain earthquake safety skills. METHODS: Participants were three students with autism spectrum disorder in a primary school special education class. We used the multiple probe model across participants to assess how digital social stories facilitated learning the « Drop, Cover, and Hold On » technique and safe evacuation. The intervention included baseline, instruction, fading, probe, follow-up, and generalization sessions. Data collection used tools developed with the skill analysis recording technique. RESULTS: Findings indicate digital social stories effectively helped all participants acquire earthquake safety skills. The intervention supported skill generalization to different settings and maintained them during follow-up sessions in the first, third, and fifth weeks post-instruction. CONCLUSION: This study shows that digital social stories can enhance the acquisition, generalization, and maintenance of safety skills in individuals with autism spectrum disorder when taught in a safe, simulated environment designed to prepare them for emergencies.

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12. Wang Y, Wang Q, Li R, Yu Y, Feng S, Wu W, Ren S. Microglial TREM2 deficiency causes E/I imbalance and triggers ASD-like behaviors by altering potassium channel Kv1.3 activation. Neurobiol Dis. 2025; 217: 107185.

Autism Spectrum Disorder (ASD) is a type of neurodevelopmental disorder characterized by deficits in social interaction and stereotyped behavior, with synaptic dysfunction playing a causal role in its pathogenesis. Microglia, as innate immune cells in CNS, are involved in regulation of synaptic transmission and plasticity through directly pruning spines and indirectly releasing bioactive substances. Interestingly, loss-of-function of triggering receptor expressed on myeloid cells 2 (TREM2), a key receptor in regulation of microglial immune functions, has been implicated in neurodevelopmental and neurodegenerative diseases through altering synaptic transmission and neuronal homeostasis. However, it is currently still not well established how TREM2 loss-of-function causes those effects. Here, we found that TREM2 deficiency during early postnatal stage led to an increased Kv1.3 channel activity in microglia, which resulted in an imbalance of excitatory and inhibitory synaptic transmissions (E/I imbalance) characterized by increased mEPSCs and reduced mIPSCs frequencies, leading to neuronal hyperactivity in neocortex. Importantly, Kv1.3 conditional knock-out and specific pharmacological inhibition effectively restored the E/I imbalance and neuronal hyperactivity, and alleviated ASD-like behaviors in TREM2-deficient mice. Together, our findings suggest that the increased Kv1.3 activity may underlie the neuronal dysfunction and behavioral deficits associated with TREM-2 deficiency, highlighting Kv1.3 as a potential therapeutic target for ASD treatment.

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