Autistic spectrum disorder (ASD) is a neurodevelopmental disorder characterized by deficits in social interactions, communication and stereotyped behaviour. Recent evidence from neuroimaging supports the hypothesis that ASD deficits in adults may be related to abnormalities in a specific frontal-temporal network [Autism-specific Structural Network (ASN)]. To see whether these results extend to younger children and to better characterize these abnormalities, we applied three morphometric methods on brain grey matter (GM) of children with and without ASD. We selected 39 sMRI images of male children with ASD and 42 typically developing (TD) from the Autism Brain Imaging Data Exchange database. We used source-based morphometry (SoBM), a whole-brain multivariate approach to identify GM networks, voxel-based morphometry (VBM), a voxel-wise comparison of the local GM concentration and surface-based morphometry (SuBM) for the estimation of the cortical parameters. SoBM showed a bilateral frontal-parietal-temporal network different between groups, including the inferior-middle temporal gyrus, the inferior parietal lobule and the postcentral gyrus; VBM returned differences only in the right temporal lobe; SuBM returned a thinning in the right inferior temporal lobe thinner in ASD, a higher gyrification in the right superior parietal lobule in TD and in the middle frontal gyrus in ASD. For the first time, we investigated the brain abnormalities in children with ASD using three morphometric techniques. The results were relatively consistent between methods, stressing the role of an Autism-specific Structural Network in ASD individuals. We also make methodological speculations on the relevance of using multivariate and whole-brain neuroimaging analysis to capture ASD complexity.
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http://dx.doi.org/10.1111/ejn.13704 | DOI Listing |
J Physiol
January 2025
Instituto de Investigaciones Cerebrales, Universidad Veracruzana, Xalapa Ver, México.
Autism spectrum disorder (ASD) is a prevalent neurodevelopmental condition affecting a substantial number of children globally, characterized by diverse aetiologies, including genetic and environmental factors. Emerging research suggests that neurovascular dysregulation during development could significantly contribute to autism. This review synthesizes the potential role of vascular abnormalities in the pathogenesis of ASD and explores insights from studies on valproic acid (VPA) exposure during neural tube development.
View Article and Find Full Text PDFPsychopharmacol Bull
January 2025
Alamiri, MD, ABPN, ScD, Al-Manara CAP Centre, Kuwait Centre for Mental Health (KCMH), Shuwaikh, State of Kuwait.
Herein, authors report on an ASD child with comorbid ADHD, ID, metabolic syndrome and nocturnal enuresis that failed multiple trials of psychotropic agents for behavioural dyscontrol. Viloxazine adjuventia brought about remarkable improvement spanning different domains. Purported pharmacodynamic mechanisms are briefly discussed.
View Article and Find Full Text PDFPsychiatry Res
December 2024
Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm Health Care Services, Karolinska University Hospital, Region Stockholm, Stockholm SE-171 76, Sweden; Stockholm Health Care Services, Region Stockholm, Sweden.
J Transl Med
December 2024
Lishui Key Laboratory of mental Health and brain Disorders, Lishui Second People's Hospital, Lishui, Zhejiang, 323000, China.
Background: Autism spectrum disorder (ASD) is a persistent neurodevelopmental disorder affecting brains of children. Mounting evidences support the associations between gut microbial dysbiosis and ASD, whereas detailed mechanisms are still obscure.
Methods: Here we probed the potential roles of gut microbiome in ASD using fecal metagenomics and metabolomics.
Mol Genet Genomic Med
January 2025
Laboratory of Ontogenetics, Research Institute of Medical Genetics, Tomsk National Research Medical Center of the Russian Academy of Sciences, Tomsk, Russia.
Background: Chromosome 3q29 duplication syndrome is a rare chromosomal disorder with a frequency of 1:5000 in patients with a neurodevelopmental phenotype. The syndrome is characterized by phenotypic polymorphism and reduced penetrance.
Methods: Patients were investigated by performing a cytogenetic analysis of GTG-banded metaphases, aCGH with the SurePrint G3 Human CGH Microarray 8×60K, qPCR, FISH, and WES.
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