Autism Research最新文献

{"title":"Autism Research: Thank You to Our 2024 Reviewers","authors":"","doi":"10.1002/aur.3310","DOIUrl":"https://doi.org/10.1002/aur.3310","url":null,"abstract":"","PeriodicalId":131,"journal":{"name":"Autism Research","volume":"18 1","pages":"9-16"},"PeriodicalIF":5.3,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143121205","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expanding Perspectives on Visual Mental Imagery in Autism: Aphantasia, Enhanced Abilities, and Future Directions","authors":"Lien-Chung Wei, Cheng-Hsien Sung","doi":"10.1002/aur.3311","DOIUrl":"10.1002/aur.3311","url":null,"abstract":"","PeriodicalId":131,"journal":{"name":"Autism Research","volume":"18 2","pages":"236-237"},"PeriodicalIF":5.3,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143069982","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"m6A-mRNA Reader YTHDF2 Identified as a Potential Risk Gene in Autism With Disproportionate Megalencephaly","authors":"Sierra S. Nishizaki,&nbsp;Nicholas K. Haghani,&nbsp;Gabriana N. La,&nbsp;Natasha Ann F. Mariano,&nbsp;José M. Uribe-Salazar,&nbsp;Gulhan Kaya,&nbsp;Melissa Regester,&nbsp;Derek Sayre Andrews,&nbsp;Christine Wu Nordahl,&nbsp;David G. Amaral,&nbsp;Megan Y. Dennis","doi":"10.1002/aur.3314","DOIUrl":"10.1002/aur.3314","url":null,"abstract":"<p>Among autistic individuals, a subphenotype of disproportionate megalencephaly (ASD-DM) seen at three years of age is associated with co-occurring intellectual disability and poorer prognoses later in life. However, many of the genes contributing to ASD-DM have yet to be delineated. In this study, we identified additional ASD-DM candidate genes with the aim to better define the genetic etiology of this subphenotype of autism. We expanded the previously studied sample size of ASD-DM individuals ten fold by including probands from the Autism Phenome Project and Simons Simplex Collection, totaling 766 autistic individuals meeting the criteria for megalencephaly or macrocephaly and revealing 154 candidate ASD-DM genes harboring <i>de novo</i> protein-impacting variants. Our findings include 14 high confidence autism genes and seven genes previously associated with DM. Five impacted genes have previously been associated with both autism and DM, including <i>CHD8</i> and <i>PTEN</i>. By performing functional network analysis, we expanded to additional candidate genes, including one previously implicated in ASD-DM (<i>PIK3CA</i>) as well as 184 additional genes connected with ASD or DM alone. Using zebrafish, we modeled a <i>de novo</i> tandem duplication impacting <i>YTHDF2</i>, encoding an N6-methyladenosine (m⁶A)-mRNA reader, in an ASD-DM proband. Testing zebrafish CRISPR knockdown led to reduced head/brain size, while overexpressing <i>YTHDF2</i> resulted in increased head/brain size matching that of the proband. Single-cell transcriptomes of <i>YTHDF2</i> gain-of-function larvae point to reduced expression of Fragile-X-syndrome-associated FMRP-target genes globally and in the developing brain, providing insight into the mechanism underlying autistic phenotypes. We additionally discovered a variant impacting a different gene encoding an m⁶A reader, <i>YTHDC1</i>, in our ASD-DM cohort. Though we highlight only two cases to date, our study provides support for the m⁶A-RNA modification pathway as potentially contributing to this severe form of autism.</p>","PeriodicalId":131,"journal":{"name":"Autism Research","volume":"18 5","pages":"966-982"},"PeriodicalIF":5.3,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/aur.3314","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143069985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cortical Thickness Differences in Autistic Children With and Without Intellectual Disability","authors":"Derek S. Andrews,&nbsp;Andrew J. Dakopolos,&nbsp;Joshua K. Lee,&nbsp;Brianna Heath,&nbsp;Devani Cordero,&nbsp;Marjorie Solomon,&nbsp;David G. Amaral,&nbsp;Christine Wu Nordahl","doi":"10.1002/aur.3313","DOIUrl":"10.1002/aur.3313","url":null,"abstract":"<p>Of the 1 in 36 individuals in the United States who are diagnosed with autism spectrum disorder, nearly 40% also have intellectual disability (ID). The cortex has been widely implicated in neural processes underlying autistic behaviors as well as intellectual ability. Thus, neuroimaging features such as cortical thickness are of particular interest as a possible biomarkers of the condition. However, neuroimaging studies often fail to include autistic individuals with ID. As a result, there are few studies of cortical thickness in autistic individuals across the entire range of intellectual abilities. This study used MRI to evaluate cortical thickness in young autistic children (<i>n</i> = 88, mean age 5.37 years) with a large range of intellectual ability (IQ 19–133) as well as nonautistic, nondevelopmentally delayed (referred to here as typically developing [TD]) peers (<i>n</i> = 53, mean age 5.29 years). We first investigated associations between full scale IQ and cortical thickness in both autistic and TD children. Autistic children had significant negative associations (i.e., thinner cortex, higher IQ) in bilateral entorhinal cortex, right fusiform gyrus, superior, middle and inferior temporal gyri, and right temporal pole that were not present in TD children. Significantly thicker cortex was also observed in these regions for autistic children with ID (i.e., IQ ≤ 70) compared with those without. Last, given the reported correspondence between the severity of autism symptoms and intellectual ability, we compared cortical thickness associations with both IQ and ADOS Calibrated Severity Scores and found these patterns overlapped to a significant degree across the cortex.</p>","PeriodicalId":131,"journal":{"name":"Autism Research","volume":"18 3","pages":"486-497"},"PeriodicalIF":5.3,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/aur.3313","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143069963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Longitudinal Symptom Burden and Pharmacologic Management of Catatonia in Autism With Intellectual Disability: An Observational Study","authors":"Joshua Ryan Smith,&nbsp;Seri Lim,&nbsp;Snehal Bindra,&nbsp;Sarah Marler,&nbsp;Bavani Rajah,&nbsp;Zachary J. Williams,&nbsp;Isaac Baldwin,&nbsp;Nausheen Hossain,&nbsp;Jo Ellen Wilson,&nbsp;D. Catherine Fuchs,&nbsp;James Luccarelli","doi":"10.1002/aur.3315","DOIUrl":"10.1002/aur.3315","url":null,"abstract":"<p>Catatonia is a highly morbid psychomotor and affective disorder, which can affect autistic individuals with and without intellectual disability. Catatonic symptoms are treatable with pharmacotherapy and electroconvulsive therapy, but the longitudinal effectiveness of these treatments in autistic individuals has not been described. We conducted a prospective observational cohort study of patients with autism and co-morbid catatonia who received outpatient care in a specialized outpatient clinic from July 1, 2021 to May 31, 2024. Data investigating pharmacologic interventions, and clinical measures including the Bush Francis Catatonia Rating Scale (BFCRS), Kanner Catatonia Severity Scale (KCS), Kanner Catatonia Examination (KCE), and Clinical Global Impression—Improvement (CGI-I) were collected. Forty-five autistic patients with co-morbid catatonia were treated during the study period. The mean age was 15.6 (SD = 7.9) years [Mdn = 16.0, range 6.0–31.0]. Forty-one patients (91.1%) met criteria for autism with co-occurring intellectual disability. All patients received pharmacotherapy. Forty-four (97.8%) were treated with benzodiazepines with a mean maximal daily dose of 17.4 mg (SD = 15.8) lorazepam equivalents. Thirty-five patients (77.8%) required more than one medication class for treatment. Sixteen (35.6%) patients received electroconvulsive therapy. Fourteen patients (31.1%) attempted to taper off benzodiazepines after achieving clinical improvement during the study period; of these, 5 patients (11.1%) were successfully tapered off, and the remaining 9 (17.8%) discontinued the taper due to a return of catatonic symptoms. Statistically significant improvement was observed across all clinical domains except the KCS. However, the majority remained at least partially symptomatic over the study period. Three patients (6.7%) died over the study period. Despite clinical improvements while receiving the gold standard for psychopharmacologic management of catatonia, chronic symptoms remained for the majority of catatonia patients over the study period, and few were able to taper and discontinue benzodiazepine treatment. Notably, the open label design of this study is a limiting factor when interpreting the results.</p>","PeriodicalId":131,"journal":{"name":"Autism Research","volume":"18 2","pages":"449-462"},"PeriodicalIF":5.3,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/aur.3315","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143048788","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"What We Publish and What We Do Not","authors":"David G. Amaral,&nbsp;the Associate Editors","doi":"10.1002/aur.3307","DOIUrl":"10.1002/aur.3307","url":null,"abstract":"&lt;p&gt;The editors of &lt;b&gt;\u0000 &lt;i&gt;Autism Research&lt;/i&gt;\u0000 &lt;/b&gt; would like to wish you a healthy, happy, and productive 2025. &lt;i&gt;If you consider publishing a paper in the journal in the future, please read the following&lt;/i&gt;:&lt;/p&gt;&lt;p&gt;During 2024, we received an unprecedented number of submissions to &lt;i&gt;Autism Research&lt;/i&gt;. We thank the authors and the reviewers for their support of the journal. We also received an unusually large number of submissions that were not consistent with the aims and scope of the journal and, therefore, were not suitable for publication in the journal. For many of these, it appears that the authors had not fully reviewed the Author Guidelines, which can be found by clicking the “Contribute” button on the blue banner on the journal home page. This takes authors to the following link (https://onlinelibrary.wiley.com/page/journal/19393806/homepage/forauthors.html).&lt;/p&gt;&lt;p&gt;To be fully informed about the types of submission most likely to be published in &lt;i&gt;Autism Research&lt;/i&gt;, we would encourage potential authors to review the instructions in full and to pay special attention to the second section “2. Aims &amp; Scope” of the Author Guidelines. &lt;b&gt;This section is there to help you determine whether your article is appropriate for the journal&lt;/b&gt;. In the text below, we summarize some of the important inclusion and exclusion criteria for submitted papers.&lt;/p&gt;&lt;p&gt;The journal focuses on reports of novel findings related to genetic, neurobiological, immunological, medical, epidemiological, and psychological mechanisms and how these influence developmental processes in autism spectrum disorder. The journal encourages the submission of original research papers (Research Articles and Short Reports) that take a developmental approach to the biology and psychology of autism, with a particular emphasis on identifying underlying mechanisms and integrating across different levels of analysis. Contributions are typically empirical, but the journal also publishes theoretical papers if they significantly advance thinking. The journal encourages papers reporting work on animal, cell, or other model systems that are directly relevant to a better understanding of autism or related conditions. The journal also publishes reports of carefully conducted clinical trials of treatments for the core symptoms or one of the common co-occurring conditions of autism.&lt;/p&gt;&lt;p&gt;For papers submitted to &lt;i&gt;Autism Research&lt;/i&gt;, a &lt;b&gt;clinical trial&lt;/b&gt; is defined as any research study that prospectively assigns human participants or groups to one or more interventions to evaluate the effects of those interventions on &lt;b&gt;health-related biomedical or behavioral outcomes&lt;/b&gt;. Health-related interventions include drugs, surgical procedures, devices, behavioral treatments, dietary interventions, or educational programs. By this definition, an equine or animal-assisted intervention would be considered a clinical trial. Health outcomes include any biomedical ","PeriodicalId":131,"journal":{"name":"Autism Research","volume":"18 1","pages":"7-8"},"PeriodicalIF":5.3,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/aur.3307","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gross Motor Development in Children With Autism: Longitudinal Trajectories From the Growing Up in New Zealand Study","authors":"Paula Araya,&nbsp;Katrina Phillips,&nbsp;Karen Waldie,&nbsp;Lisa Underwood","doi":"10.1002/aur.3304","DOIUrl":"10.1002/aur.3304","url":null,"abstract":"<p>This study explored gross motor development (GMD) trajectories among 6359 children, with and without autism, from the <i>Growing Up in New Zealand</i> longitudinal cohort study. By the age of 8, 173 children had either an autism diagnosis (<i>n</i> = 108) or parent-reported autism concerns (<i>n</i> = 65). Gross motor milestones were reported by mothers when children were 9, 24, and 54 months of age. We found that irrespective of autism diagnosis, GMD delays at 24 months of age were more likely among girls, children born preterm, and those whose mothers identified as European. A mixed-effect logistic regression model, controlling for antenatal maternal and child covariates, revealed that the proportion of children with GMD delay (relative to their peers) increased significantly from 9 to 54 months for all three groups, but the increase was greater for those with autism concerns (OR = 1.28, 95% CI = 1.08–1.52) or an autism diagnosis (OR = 1.26, 95% CI = 1.10–1.43) compared to the no autism group (OR = 1.06, 95% CI = 1.02–1.10). Differences in the changes in GMD performance among children with an autism diagnosis compared to those without autism occurred between 9 and 24 months (OR = 2.16, 95% CI = 1.13–4.13). No significant GMD delay differences were found at any time between children with an autism diagnosis versus those with autism concerns. Children with a GMD delay should be screened for autism at 24 m. Early identification is the first step toward knowledge-based, effective intervention of developmental difficulties.</p>","PeriodicalId":131,"journal":{"name":"Autism Research","volume":"18 2","pages":"437-448"},"PeriodicalIF":5.3,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/aur.3304","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Naa15 Haploinsufficiency and De Novo Missense Variants Associate With Neurodevelopmental Disorders and Interfere With Neurogenesis and Neuron Development","authors":"Mei He,&nbsp;Bing Du,&nbsp;Guodong Chen,&nbsp;Yongqing Lyu,&nbsp;Hui Guo,&nbsp;Xiangbin Jia,&nbsp;Kun Xia","doi":"10.1002/aur.3308","DOIUrl":"10.1002/aur.3308","url":null,"abstract":"<div>\u0000 \u0000 <p>Neurodevelopmental disorders (NDDs) encompass a group of conditions that impact brain development and function, exhibiting significant genetic and clinical heterogeneity. NAA15, the auxiliary subunit of the N-terminal acetyltransferase complex, has garnered attention due to its association with NDDs. However, the precise role of <i>NAA15</i> in cortical development and its contribution to NDDs remain elusive. By employing targeted sequencing on a large Chinese cohort affected by ASD and conducting an extensive literature review, we have compiled 64 distinct variants in the <i>NAA15</i> gene identified among individuals with neurodevelopmental disorders. Our research demonstrates that loss of NAA15 leads to a substantial increase in neuronal count, potentially resulting in aberrant brain development and triggering repetitive as well as anxious behaviors in mice models. Furthermore, disorder-associated variants within <i>NAA15</i> impair axon and synapse formation processes crucial for neural connectivity establishment. These findings shed light on the consequences of NAA15 deficiency along with its de novo mutations on brain development while unraveling the cellular mechanisms underlying NDDs.</p>\u0000 </div>","PeriodicalId":131,"journal":{"name":"Autism Research","volume":"18 5","pages":"954-965"},"PeriodicalIF":5.3,"publicationDate":"2025-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143017295","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Demographic Correlates of Autism: How Do Associations Compare Between Diagnosis and a Quantitative Trait Measure?","authors":"Kristen Lyall,&nbsp;Aisha S. Dickerson,&nbsp;Annette M. Green,&nbsp;Seth Frndak,&nbsp;Lisa A. Croen,&nbsp;Jennifer L. Ames,&nbsp;Lyndsay A. Avalos,&nbsp;Judy L. Aschner,&nbsp;Nicole R. Bush,&nbsp;Carlos A. Camargo Jr,&nbsp;Viren D'Sa,&nbsp;Stephen R. Dager,&nbsp;Anne L. Dunlop,&nbsp;Assiamira Ferrara,&nbsp;Jody M. Ganiban,&nbsp;James E. Gern,&nbsp;Tre D. Gissandaner,&nbsp;J. Carolyn Graff,&nbsp;Irva Hertz-Picciotto,&nbsp;Alison E. Hipwell,&nbsp;Tengfei Ma,&nbsp;Meghan Miller,&nbsp;Laura Murphy,&nbsp;Margaret R. Karagas,&nbsp;Rachel S. Kelly,&nbsp;Amy Margolis,&nbsp;Daphne Koinis-Mitchell,&nbsp;Cindy T. McEvoy,&nbsp;Daniel Messinger,&nbsp;Ruby Nguyen,&nbsp;Emily Oken,&nbsp;Sally Ozonoff,&nbsp;Grier P. Page,&nbsp;Susan L. Schantz,&nbsp;Rebecca J. Schmidt,&nbsp;Coral L. Shuster,&nbsp;Julie B. Schweitzer,&nbsp;Stephen J. Sheinkopf,&nbsp;Joseph B. Stanford,&nbsp;Cindy O. Trevino,&nbsp;Scott T. Weiss,&nbsp;Heather E. Volk,&nbsp;Robert M. Joseph,&nbsp;program collaborators for Environmental influences on Child Health Outcomes","doi":"10.1002/aur.3296","DOIUrl":"10.1002/aur.3296","url":null,"abstract":"<div>\u0000 \u0000 <p>Prevalence of autism diagnosis has historically differed by demographic factors. Using data from 8224 participants drawn from the Environmental influences on Child Health Outcomes (ECHO) Program, we examined relationships between demographic factors and parent-reported autism-related traits as captured by the Social Responsiveness Scale (SRS; <i>T</i> score &gt; 65) and compared these to relations with parent-reported clinician diagnosis of ASD, in generalized linear mixed effects regression analyses. Results suggested lower odds of autism diagnosis, but not of SRS <i>T</i> &gt; 65, for non-Hispanic Black children (adjusted odds ratio [OR] = 0.76, 95% CI 0.55, 1.06) relative to non-Hispanic White children. Higher maternal education was associated with reduced odds of both outcomes (OR = 0.73, 95% CI 0.51, 1.05 for ASD autism diagnosis and 0.4, 95% CI 0.29, 0.55 for SRS score). In addition, results suggested a lower likelihood of autism diagnosis but a higher likelihood of an SRS score &gt; 65 in Black girls. Findings suggest lower diagnostic recognition of autism in non-Hispanic Black children, despite a similar degree of SRS-assessed autism-related traits falling in the clinically elevated range. Further work is needed to address this disparity.</p>\u0000 </div>","PeriodicalId":131,"journal":{"name":"Autism Research","volume":"18 3","pages":"648-659"},"PeriodicalIF":5.3,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142959796","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relationship between service receipt during the COVID-19 pandemic and autistic children's multisystem outcomes and autism severity: A SPARK dataset analysis","authors":"Jung-Mei Tsai,&nbsp;Anjana Bhat","doi":"10.1002/aur.3256","DOIUrl":"10.1002/aur.3256","url":null,"abstract":"<p>Children with autism spectrum disorder (ASD) display a variety of core and co-occurring difficulties in social, communication, everyday functioning, cognitive, motor, and language domains. Receiving a combination of services to accommodate needs of autistic individuals is essential for improving their future outcomes. During the COVID-19 pandemic, reduced service access negatively impacted autistic children's outcomes. This study aimed to examine the relationship between service receipt and parental perceived outcomes in autistic children while accounting for various demographic, child, and parental factors. We utilized parental COVID-19 impact survey data from the SPARK study (<i>N</i> = 6067). Ordinal logistic regression analyses were used to predict perceived child outcomes. Demographic, child, and parental factors were included in the prediction models. Service receipt of SLT, ABA, PT/OT, MED, and MH were associated with perceived child outcomes. PT/OT and ABA predicted improvements in domains of social interaction, everyday activity, and overall autism severity; SLT and ABA contributed to improved perceived communication outcomes. Receiving MH and MED services was associated with worsening of perceived outcomes on all domains. Younger age, males, higher family income, lower autism severity, lower motor, function, and cognitive delay, greater language delay, and the absence of parental mental health issues were associated with greater improvements in various perceived outcomes. Overall, PT/OT and ABA services are associated with improved perceived social and functional outcomes whereas SLT and ABA services are associated with improved perceived communication outcomes. We also provide a wholistic view of factors affecting relationships between service receipt and perceived child outcomes during the pandemic.</p>","PeriodicalId":131,"journal":{"name":"Autism Research","volume":"18 1","pages":"217-229"},"PeriodicalIF":5.3,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143069988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}