Individuals with autism spectrum disorder (ASD) commonly display speech processing abnormalities. Binding of acoustic features of speech distributed across different frequencies into coherent speech objects is fundamental in speech perception. Here, we tested the hypothesis that the cortical processing of bottom-up acoustic cues for speech binding may be anomalous in ASD. We recorded magnetoencephalography while ASD children (ages 7-17) and typically developing peers heard sentences of sine-wave speech (SWS) and modulated SWS (MSS) where binding cues were restored through increased temporal coherence of the acoustic components and the introduction of harmonicity. The ASD group showed increased long-range feedforward functional connectivity from left auditory to parietal cortex with concurrent decreased local functional connectivity within the parietal region during MSS relative to SWS. As the parietal region has been implicated in auditory object binding, our findings support our hypothesis of atypical bottom-up speech binding in ASD. Furthermore, the long-range functional connectivity correlated with behaviorally measured auditory processing abnormalities, confirming the relevance of these atypical cortical signatures to the ASD phenotype. Lastly, the group difference in the local functional connectivity was driven by the youngest participants, suggesting that impaired speech binding in ASD might be ameliorated upon entering adolescence.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9898310 | PMC |
http://dx.doi.org/10.1016/j.nicl.2023.103336 | DOI Listing |
Eur J Med Genet
December 2024
First Department of Neurology, First Affiliated Hospital of Kunming Medical University, Kunming, 650000, China. Electronic address:
The Chromodomain Helicase DNA-binding (CHD) protein family is ATP-dependent chromatin remodeling proteins that utilize energy produced by ATP hydrolysis to regulate chromatin structure and thereby modulate gene expression. The earliest report of a CHD3 gene mutation was by O'Roak, who found it during whole exome sequencing of 189 autism families in 2012. In 2018, Snijders Blok systematically assessed the autosomal dominant neurodevelopmental disorder caused by CHD3 gene damage, known as Snijders Blok-Campeau syndrome (SNIBCPS, OMIM 618205).
View Article and Find Full Text PDFBrain Commun
December 2024
Laboratory for Neuropathology, Department of Imaging and Pathology, KU Leuven, Leuven 3000, Belgium.
Misfolded α-synuclein protein accumulates in 43-63% of individuals with symptomatic Alzheimer's disease. Two main patterns of comorbid α-synuclein pathology have been identified: caudo-rostral and amygdala-predominant. α-Synuclein aggregates have been shown to interact with the transactive response DNA-binding protein 43 (TDP-43) and abnormally phosphorylated tau protein.
View Article and Find Full Text PDFAgeing Res Rev
January 2025
Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA; Nutritional Sciences Department, College of Human Sciences, Texas Tech University, Lubbock, TX 79409, United States; Department of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA; Department of Neurology, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA 5. Department of Public Health, Graduate School of Biomedical Sciences, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA; Department of Speech, Language, and Hearing Sciences, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA. Electronic address:
Brief Bioinform
November 2024
Key Laboratory of Structural Biology of Zhejiang Province, School of Life Sciences and Research Center for Industries of the Future, Westlake University, 600 Dunyu Road, Xihu District, Hangzhou, Zhejiang 310030, China.
J Pediatr
November 2024
Department of Global Health, Boston University School of Public Health, Boston, MA.
Objective: To examine cross-sectional relationships between biomarkers of environmental enteric dysfunction (EED), an acquired subclinical condition of the small intestine, and anthropometric and developmental outcomes among children in Lusaka, Zambia.
Study Design: Serum samples were collected from 240 children aged 27 to 35 months enrolled in a cluster-randomized trial assessing the effects of growth charts and small-quantity lipid-based nutrient supplements on linear growth. Samples were analyzed using the 11-plex Micronutrient and EED Assessment Tool, which incorporates 2 biomarkers of EED, namely intestinal fatty acid-binding protein (I-FABP), a marker of epithelial damage, and soluble CD14 (sCD14), a marker of microbial translocation.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!