Pubmed du 08/10/25
1. Al-Omari A, Mohiuddin S. Identification and Treatment of Catatonia Presenting as Agitation and Self Injury in an Adolescent With Rett Syndrome. Case Rep Psychiatry. 2025; 2025: 9715900.
Catatonia is a complex psychomotor syndrome associated with several psychiatric disorders, including schizophrenia and autism. It is also associated with neurologic conditions such as encephalitis and epilepsy. Catatonia has also been described in genetic syndromes such as Down Syndrome. Catatonia presents with two main subtypes. Retarded catatonia is characterized by stupor, immobility, mutism, rigidity, and withdrawal, as well as negativism, posturing, and echolalia/echopraxia. Excited catatonia is primarily characterized by psychomotor agitation and occasionally self-injurious behaviors. Though the pathophysiology of catatonia remains poorly understood, treatment with benzodiazepines is effective in many cases, with electroconvulsive therapy indicated in cases of poor response. Rett syndrome is an X-linked neurodevelopmental disease associated with mutations in methyl-CpG-binding protein 2 and is characterized by regression of spoken language and purposeful hand skills, gait abnormalities, and stereotyped hand movements. Herein we describe a case of catatonia associated with Rett syndrome in a 17-year-old female. Her presentation was notable for hyperactivity, impulsive behaviors, agitation, self-injurious behaviors, and aggression. The patient had limited response to multiple medication trials. Initially she had a positive response to treatment with lorazepam, with later waning efficacy despite dose escalation. The patient was admitted to the inpatient psychiatry and completed an index course of 13 ECT treatments followed by maintenance ECT, completing 30 treatments in total. Treatment resulted in significant improvements in self-injurious behaviors, agitation, and overall engagement. In conclusion, catatonia should be considered in individuals with Rett syndrome who present with agitation and self-injury to aid in overall symptom improvement and outcome.
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2. Bruno G, Lindblom A, Tupou J, Kewene F, Waisman TC, Magiati I. Decolonizing autism research: Integrating indigenous ways of knowing, being, and doing. Autism. 2025: 13623613251382398.
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3. Cibralic S, Barker L, Hawker P, Tonge B, Williams K, Elliott EJ, Bellgrove M, Silk T, Anderson V, Kohn M, Sciberras E, Eapen V. Systematic review: the impact of policy levers on mental health service utilization and access for Autistic children. Child Adolesc Psychiatry Ment Health. 2025; 19(1): 109.
OBJECTIVE: Autistic children’s ability to access mental health services can be challenging due to the limited availability of therapists with autism experience, service ineligibility, and financial strain. This systematic review evaluated and synthesized literature regarding the impact of government policy levers on the access to, and utilization of, mental health services by Autistic children and their families. METHOD: Interdisciplinary databases together with gray literature and supplementary searches were used to identify relevant articles. Peer-reviewed, English language studies which reported on the impact of government policy levers on the utilization of, and access to, mental health services by Autistic children and their families were included. RESULTS: Searches resulted in the identification of 2305 articles (database searches = 744, additional searches = 1531), six of which were included in the final review. All six articles were from the United States of America, published between 2013 and 2020, with a focus on national and state regulatory policy levers targeting insurance companies. Results indicated that most policy levers did not improve service access to, or utilization of, mental health services. Gray literature searches identified that several countries had implemented autism specific policy levers, most however had not been evaluated regarding their impact on mental health service access and utilization by Autistic children or their families. CONCLUSION: The majority of identified policy levers have not resulted in greater utilization or access of mental health services for Autistic children or their families. More global research, focusing on datasets that have allowed policies time to impact change, is needed.
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4. Fekih-Romdhane F, Chaibi LS, Alhuwailah A, Sakr F, Helmy M, Shuwiekh HAM, Boudouda NE, Zarrouq B, Naser AY, Jebreen K, Roubi ML, Hassan ARB, Merdad N, Amin R, Nawajah I, Mohammed AH, Farhan SS, AlAni OA, Dabbous M, Malaeb D, Obeid S, Loch AA, Cheour M, Hallit S. Correction: Loneliness and susceptibility to social pain mediate the association between autistic traits and psychotic experiences in young non-clinical adults. Sci Rep. 2025; 15(1): 35036.
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5. Geng J, Wang X, Pan J, Khan D, Pimcharoen S, Zhang Y, Mosammaparast N, Hirose S, Petrucelli L, Brandman O, Qi LS, Lu B. CRISPR activation of the ribosome-associated quality control factor ASCC3 ameliorates fragile X syndrome phenotypes in mice. Sci Transl Med. 2025; 17(819): eadq3551.
Loss of fragile X messenger ribonucleoprotein (FMRP) causes fragile X syndrome (FXS), an inherited neurodevelopmental disorder resulting in intellectual disability and autism spectrum disorder; however, the molecular function of FMRP remains uncertain. Here, using cell lines and fibroblasts and induced pluripotent stem cell-derived neurons from healthy individuals and patients with FXS, we showed that FMRP regulates collided ribosomes by recruiting activating signal cointegrator 1 complex subunit 3 (ASCC3), an early-acting ribosome-associated quality control (RQC) factor to collided ribosomes, and either positively or negatively regulating translation, depending on transcript context. Disease-associated ASCC3 variants that perturbed ASCC3-FMRP interaction were also found to be defective in ribosome association and handling of collided ribosomes. In cells of a patient with FXS and the Fmr1 KO mouse model, ASCC3 abundance was reduced, and overexpression of ASCC3 in the brains of fetal Fmr1 KO mice promoted neuronal migration. In addition, CRISPR-mediated activation of ASCC3 by lateral ventricular injection of adeno-associated virus (AAV) ameliorated synaptic defects and improved locomotor activity, cognitive deficits, obsessive-compulsive-like behavior, and social interaction deficits after 1 month in 2-month-old Fmr1 KO mice compared with untreated Fmr1 KO controls. In conclusion, these data implicated FMRP in the handling of collided ribosomes to maintain protein homeostasis during neurodevelopment and synaptogenesis and demonstrated proof of concept that targeting RQC may offer alternative treatment strategies for FXS.
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6. Liang SF, Ming Y, Huang HT, Lo RY, Chompoopong S, Chen CC, Liu IY. Activation of GABA transmission by clonazepam reverses the autistic-like phenotypes of the Cav3.2 knockout mice. Neurotherapeutics. 2025: e00761.
Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by social and communication deficits, accompanied by restricted and repetitive behaviors. ASD is a lifelong condition that causes a heavy medical and societal burden. To date, there are no disease-modifying, mechanism-targeted treatments approved for core ASD symptoms. In human studies, loss-of-function mutations in the CACNA1H gene, which encodes the T type Cav3.2 calcium channel, have been associated with ASD. However, animal and molecular studies investigating the underlying mechanism in ASD patients with CACNA1H mutations are lacking. In this study, we performed a series of behavioral assays to phenotype the Cav3.2 systemic knockout (Cav3.2KO) mice. The Cav3.2KO mice exhibited ASD-like behaviors, including impaired social novelty, increased self-grooming behavior, and deficits in recognition and retrieval of fear memory. Notably, enhancing γ-aminobutyric acid (GABA) signaling via administration a low-dose of clonazepam (CLZ) rescued these behavioral impairments in the Cav3.2KO mice. Furthermore, we found that the intrinsic GABA level was significantly reduced in the frontal cortex of Cav3.2KO mice, suggesting that GABA transmission was impaired in the Cav3.2KO mice. Together, our findings suggest that loss-of-function in the Cav3.2 channel contributes to ASD-like phenotypes through disrupted GABAergic signaling and that pharmacological enhancement of GABAergic signaling may offer a potential therapeutic approach for individuals with ASD carrying the CACNA1H mutations.
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7. Liu D, Tao K, Sun Y, Hao J, Wang S. The role of the Wnt/BDNF pathway in maternal SCH-induced autism-like phenotypes in offspring rats: behavioral and molecular mechanisms. Transl Psychiatry. 2025; 15(1): 387.
Maternal subclinical hypothyroidism (SCH) has been associated with neurodevelopmental disorders, but the molecular mechanisms underlying its impact on offspring behavior remain poorly understood. This study investigates the role of the Wnt/BDNF signaling pathway in the development of autism-like behaviors in male offspring rats born to SCH mothers. Our findings demonstrate that maternal SCH induces significant behavioral abnormalities in the offspring, including increased grooming behavior and deficits in social interaction, which are hallmarks of autism spectrum disorder (ASD). These behaviors correlate with alterations in hippocampal protein expression, particularly a decrease in Brain-Derived Neurotrophic Factor (BDNF) and key signaling molecules involved in neuronal survival, such as cAMP response element-binding protein (CREB) and B-cell lymphoma 2 (Bcl-2). Additionally, we observe a marked upregulation of mTOR gene expression and a downregulation of Wnt signaling in the hippocampus of SCH-exposed offspring. These molecular changes are consistent with disrupted synaptic plasticity and neurogenesis, which are critical processes for cognitive and social development. Our study further reveals that impaired Wnt/BDNF signaling may play a pivotal role in the pathogenesis of autism-like behaviors in these offspring. Moreover, sex-specific differences were observed in the behavioral manifestations, with male offspring showing more pronounced deficits, suggesting a gender-dependent sensitivity to maternal SCH. This research provides novel insights into the molecular pathways by which maternal thyroid dysfunction contributes to neurodevelopmental disorders, offering potential targets for therapeutic intervention.
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8. Lopes LPN, Boeira LDS, Figueiredo Modesto AC, Ramos-Silva A, Menin VP, Abe FC, Lopes LC. Barriers to mental health services for children and adolescents with autism spectrum disorder in Brazil: protocol for a qualitative evidence synthesis and citizen panel (BARRIER-Free-BR Project). BMJ Open. 2025; 15(10): e107543.
INTRODUCTION: The perspectives of stakeholders directly affected by mental health services for autism spectrum disorder (ASD) are essential for the quality of these services. However, it is crucial that these perspectives are informed by the best available evidence and adapted to the local context. This study aims to analyse barriers related to mental health services for children and adolescents with ASD from the perspective of families and caregivers, considering social, racial and gender aspects. METHODS: Three steps will be taken: stakeholder engagement through an online meeting to refine the research question and understand the magnitude of the problem; (b) qualitative evidence synthesis using five databases and grey literature to identify studies that have collected and analysed qualitative data on barriers to mental health services for children and adolescents with ASD in Brazil. Only studies conducted in Brazil that consider the perspectives of family members and caregivers will be included. (c) A citizen panel with families of children and adolescents with ASD will be used to discuss and validate the synthesis findings. ETHICS AND DISSEMINATION: We will provide a set of evidence-informed and stakeholder-experienced barriers to mental health services for children with ASD in Brazil. This represents an effort to engage stakeholders in evidence descriptions to inform policy. We plan to disseminate the findings through various means, including peer-reviewed journal publications, presentations at national conferences, invited workshops and webinars, patient associations and academic social media platforms. The project was approved by the Ethics Committee for Research at the University of Sorocaba (approval number 78747224.7.0000.5500). TRIAL REGISTRATION NUMBER: Open Science Framework-10.17605/OSF.IO/DVAKG.
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9. Melinda M, Purnamasari PD, Fahmi F, Sinulingga EP, Muliyadi M, Away Y, Yunidar Y, Juwono FH. A comprehensive EEG dataset and performance assessment for Autism Spectrum Disorder. Sci Rep. 2025; 15(1): 34981.
Autism Spectrum Disorder (ASD) diagnosis can greatly benefit from more efficient and accurate tools to enable early intervention and reduce long-term healthcare costs associated with delayed diagnosis. Electroencephalography (EEG) has emerged as a promising non-invasive technique for detecting neural patterns linked to ASD. This research evaluates the effectiveness of three preprocessing techniques, Butterworth, Discrete Wavelet Transform (DWT), and Independent Component Analysis (ICA), in enhancing EEG signal quality for ASD classification. The performance of each method is assessed using Signal-to-Noise Ratio (SNR), Mean Absolute Error (MAE), Mean Squared Error (MSE), Spectral Entropy (SE), and Power Spectral Density (PSD) analysis to explore frequency band distribution. Additionally, Hjorth parameters-activity, mobility, and complexity-are computed to capture neural dynamics associated with ASD. Results showed that ICA achieved the highest SNR values (normal: 86.44, ASD: 78.69), indicating superior denoising capability, while DWT offered the lowest error metrics (MAE: 4785.08, MSE: 309,690 for ASD), demonstrating its robustness in preserving signal characteristics. Butterworth provided moderate results across metrics. Notably, Hjorth parameters revealed that neurotypical EEGs exhibited higher activity and complexity, highlighting distinct neural dynamics compared to ASD. These findings suggest that ICA is optimal for applications prioritizing signal clarity, while DWT offers a balanced approach for feature preservation in ASD EEG analysis. These findings are expected to support the development of more accurate, EEG-based diagnostic tools for ASD that can be integrated into clinical decision support systems and early screening programs.
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10. Močnik S, Gregorič Kumperščak H, Demšar A. Case Report: A complex case of an adolescent female with comorbid borderline personality disorder and autism spectrum disorder. Front Psychiatry. 2025; 16: 1681412.
Diagnosing borderline personality disorder (BPD) and autism spectrum disorder (ASD) in adolescent females presents significant challenges due to the overlap in their symptomatology. Both conditions share features such as emotional dysregulation, impulsivity, and difficulties in interpersonal relationships, making differentiation crucial yet difficult. This case report examines an adolescent female with co-occurring BPD and ASD, emphasizing the complexities of distinguishing between the two. It explores the role of developmental history, behavioral patterns, and neurobiological factors in forming a precise diagnosis. Additionally, the report highlights the impact of comorbid conditions like depression and anxiety, which frequently accompany both BPD and ASD, further complicating the diagnostic process. By focusing on this case, we underscore the importance of a thorough, multidimensional diagnostic approach to ensure accurate identification and treatment. The case serves as a reminder of the need for heightened awareness of how BPD and ASD can present in females and advocates for more nuanced diagnostic tools and tailored interventions to improve clinical outcomes for this population.
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11. Narducci C, Donno F, Milone A, Placini F, Glennon JC, Masi G, Coghill D, Zuddas A, Carucci S, Balia C. Emotional dysregulation, executive functions and callous-unemotional traits in children and adolescents with Oppositional Defiant Disorder/Conduct Disorder and Autism Spectrum Disorder: a direct comparison. J Psychiatr Res. 2025; 191: 507-15.
BACKGROUND: Autism Spectrum Disorder (ASD), Oppositional Defiant Disorder (ODD) and Conduct Disorder (CD) share many symptomatic dimensions. Emotional dysregulation (ED) and Callous-Unemotional (CU) traits have been described as transdiagnostic symptoms as well as executive dysfunctions. However, few previous studies compared these disorders directly at a clinical and a neuropsychological level. METHODS: 138 children and adolescents aged 10-17 years (n = 63 ODD/CD; n = 35 ASD and n = 40 TDC), with an intelligence quotient ≥80 were included. The three groups were compared on the emotional and behavioural characteristics by the CBCL 6-18 questionnaire (with particular attention to the emotional dysregulation profile), on the CU traits assessed by the ICU questionnaire (parent version), and the executive functioning assessed by the BRIEF parent form. RESULTS: Compared to controls, ODD/CDs and ASDs, showed a higher proportion of internalizing and externalizing symptoms, greater emotional dysregulation, higher presence of callous-unemotional traits and executive dysfunction. While participants with ODD/CD significantly differed from those with ASD with higher deficits in impulse inhibition as well as greater planning and organization problems, the two populations did not differ in working memory or the ability to initiate or shift as measured by the BRIEF. ED was confirmed as a transdiagnostic symptom, though more highly represented in ODD/CD compared to ASD. CU traits were also seen as cross-disorder problems, confirming deficits in empathy across both disorder groups, albeit with somewhat different profiles: ODD/CDs showed greater callousness and uncaring than ASDs, while they did not statistically differ from them in the unemotionality. CONCLUSIONS: Our study provides a better understanding of the clinical and neuropsychological character of ODD/CD and ASD populations, showing that they present as overlapping entities but with some specific features.
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12. Pérez-Fuster P, Herrera G, Vera L, Nadel J, Tijus C, López-Fernández A, Stancheva M, Kozareva Y, Andreeva A, Büyüksoylu S, Avşar A, Koçak E, Leppink J. Pictogram room augmented reality technology games improve body knowledge, imitation, and joint attention skills in autistic children with intellectual disability. Sci Rep. 2025; 15(1): 34966.
Body knowledge, imitation, and joint attention are foundational for child development, yet many autistic children with intellectual disability struggle to acquire these skills. This study evaluated the effects of an educational intervention using Pictogram Room (PR), an open-access augmented reality (AR) technology program with games targeting these abilities. Twenty-three autistic children with intellectual disability (ages 7-14) from Spain, Bulgaria, and Türkiye participated. A stepped wedge randomized design was implemented across two groups. Over 27 sessions, delivered in their usual educational settings by their regular staff, participants showed significant and sustained improvements in body knowledge, imitation, and joint attention. This is the first AR-based intervention shown to simultaneously enhance these three core skills in this population. The program is brief, socially valid, and requires no specialized training, making it a promising tool for inclusive educational practice.
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13. Si Y, Zhang H. Structure-function coupling reveals the excitation-inhibition imbalance in autism spectrum disorder: A perspective from large-scale whole-brain network modeling. Chaos. 2025; 35(10).
Excitation-inhibition (E-I) imbalance is a core pathological mechanism in autism spectrum disorder (ASD). However, current research on how E-I balance changes in ASD remains highly controversial. In this study, we integrate structural and functional magnetic resonance imaging data from the UCLA Multimodal Connectivity Database to construct a large-scale whole-brain network model, aiming to investigate the potential neural mechanism of E-I imbalance in ASD. We find that compared with healthy controls, patients with ASD exhibit stronger structural-functional connectivity (SC-FC) coupling, suggesting impaired cognitive flexibility. Model analysis demonstrates altered network dynamics in ASD, characterized by reduced optimal coupling strength between empirical and simulated FC and a lower small-world index in simulated functional networks. Furthermore, a marked shift in neural oscillations is observed in ASD, including increased activity in the δ band and decreased activity in the α band, consistent with clinical findings. More importantly, our study reveals heterogeneous reductions of the E-I ratio in ASD across multiple spatial scales, spanning from local brain regions to large-scale networks, particularly highlighting a significant negative correlation between E-I ratio and SC-FC coupling. These findings establish a direct link between E-I dysregulation and abnormal structure-function integration in brain networks, providing novel insights into the complex pathogenesis underlying ASD.
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14. Sturm KL, Semak D, Scheier ZA, Ramos RL, Otazu GH. Odor experience stabilizes glomerular output representations in two mouse models of autism. eNeuro. 2025.
Novel stimuli can be stressful for individuals with Autism Spectrum Disorders (ASD), though repeated exposure can reduce this effect. In Cntnap2(-/-) and Shank3B(+/-) mouse models of ASD, novel background odors impaired behavioral target odor recognition but that deficit improved with training. To investigate the neural basis of this improvement, we used widefield calcium imaging to measure olfactory bulb responses in Cntnap2(-/-) and Shank3B(+/-) mice and WT mice of either sex. Training with background odors enhanced both behavioral performance and neural discriminability of odor mixtures in both Cntnap2(-/-) and Shank3B(+/-) as well as WT mice. Naïve Cntnap2(-/-) and Shank3B(+/-) mice showed greater trial-to-trial neural variability than WT mice, but training stabilized neural responses. Critically, training produced a widespread reduction in olfactory bulb responses to background odors in ASD models, but not in WT mice. Thus, despite similar behavioral improvements as WT mice, Cntnap2(-/-) and Shank3B(+/-) mice relied on a distinct broad suppression of background odor responses to enhance olfactory coding in the presence of background odors.Significance Statement Abnormal sensory responses to unfamiliar stimuli are a hallmark of Autism Spectrum Disorders (ASD) and can be alleviated with prolonged exposure. Neural variability in sensory responses is observed in both individuals with ASD and different mouse models, but its impact on behavior remains unclear. Using two ASD-associated gene mutation models (Shank3 and Cntnap2), we performed widefield calcium imaging in the olfactory bulb. Prolonged exposure to a background odor stabilized olfactory bulb activity, enhancing neural coding and discrimination in these two different mouse models of ASD, but not in WT mice, despite similar improvements in behavior. This work highlights how neural activity fluctuations in the olfactory bulb influence behavior in ASD, offering insights into sensory processing mechanisms and potential therapeutic strategies.
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15. Suder A, Nawrot J, Kulesa-Mrowiecka M, Zyznawska J, Gniadek A. Diagnostic tools used to assess the functional development of 2-year-old children born prematurely. Folia Med Cracov. 2025; 65(1): 99-106.
In Poland, preterm infants account for 6-7% of all births. Preterm deliveries are associated with a number of short- and long-term health conditions and therefore pose a major public health challenge. Monitoring the psychomotor development of children born prematurely is a significant challenge for pediatricians and neonatologists. Early diagnosis of delayed functional development enables timely therapeutic intervention by developmental specialists, such as physiotherapists, educators, psychologists, and speech therapists. Currently, monitoring the development of preterm infants during the first year of life is common practice. However, due to the significant percentage of late preterm infants in the population of prematurely born newborn population, there is a justified need to focus on the periodic assessment of their functional development also beyond the first year of life. Regular and multidimensional developmental monitoring in this group of patients is crucial due to the increased risk of subtle but clinically significant developmental delays that may manifest at later stages of life.
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16. Sundarimaa E, Chan SP, Zheng RM, Chong SC, Aishworiya R. Association Between Screen Time Exposure and Scores on the Modified Checklist for Autism in Toddlers, Revised With Follow-Up (M-CHAT-R/F) in Children From a Multi-ethnic Population-Based Sample in Singapore. J Autism Dev Disord. 2025.
PURPOSE: Despite the growing evidence suggesting an association between screen time exposure (STE) in children and autism symptoms, a thorough understanding of this including the directionality, especially among the general child population is lacking. We aimed to determine the associations, if any, between STE and results on the Modified Checklist for Autism in Toddlers, Revised with Follow-Up (M-CHAT-R/F) in children from a multi-ethnic population-based sample in Singapore. METHODS: This cross-sectional study included children (1) between 17 and 24 months of age and (2) typically developing with no known developmental conditions, attending routine visits in primary care. Caregivers reported daily screen time via a questionnaire and completed the M-CHAT-R/F (standard administration protocol followed). Logistic and linear regression analyses and structured equation modelling including covariates were conducted. RESULTS: The sample comprised 5,336 multi-ethnic children (mean age 18.6 ± 0.9 months, 64.2% Chinese ethnicity, 23.9% Malay, 5.8% Indian). Mean STE was 1.31 ± 1.33 h/day. Increased STE was associated with a higher likelihood of a positive M-CHAT-R/F screen (OR = 1.24, 95% CI [1.01, 1.53], p < 0.05). Higher STE was associated with greater odds of having a response of concern for the social-communication questions but not those on motor/sensory aversion. Both the final M-CHAT-R/F score and the screening outcome was directly explained by STE in the structural equation model (β = 0.05, 95% CI [0.03, 0.07], p < 0.001 and OR = 1.24, 95% CI [1.01, 1.53], p < 0.05). CONCLUSION: Findings suggest a significant association between higher STE and autism symptoms, especially related to social communication. Evaluation and support of children with a positive M-CHAT-R/F screening result should include addressing STE and mitigating exposure.
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17. Zoga K, Villiere S, Tikiyani V, Edwards-Cintron AF, Thokachichu P, Nicodemus P, Camara PG, Hart MP. Multiple autism genes influence GABA neuron remodeling via distinct developmental trajectories. Genetics. 2025; 231(2).
Variation in over 100 genes is now associated with increased risk for autism and related neurodevelopmental conditions, but how this variation results in distinct and overlapping behavioral changes is still not well understood. Recent efforts have focused on screening many autism genes at once for functional and phenotypic convergence, and identified subsets that are crucial for many early steps of neurodevelopment. Few studies have screened later steps of neurodevelopment, circuit function, circuit plasticity, or behaviors. We screened 20 conserved autism-associated genes for impact on experience-dependent neuron remodeling in Caenorhabditis elegans. Loss of unc-44/ANK2, set-4/KMT5B, daf-18/PTEN, gap-2/SYNGAP1, and chd-1/CHD2/8 increased, while unc-36/CACNA2D3 decreased, neurite outgrowth of the GABAergic DVB neuron in adults. Although daf-18/PTEN, set-4/KMT5B, and unc-44/ANK2 had convergent phenotypes, they arise from distinct temporal trajectories with differential impact on DVB presynaptic morphology. Screening for the DVB regulated spicule protraction behavior identified multiple autism genes involved, but only unc-44/ANK2 and unc-36/CACNA2D3 were shared between screens. Application of a metric geometry computational framework (CAJAL) to the DVB morphology dataset identified 5 additional genes that impact DVB morphology, including unc-2/CACNA1A and unc-10/RIMS1, which also significantly impacted behavior. This work defines new regulators and molecular mechanisms of experience-dependent neuron remodeling and circuit plasticity, and further links these processes with conserved autism genes. It also demonstrates the utility of using intact, behavior generating circuits in C. elegans, to screen for novel roles for conserved autism genes.