Despite enthusiasm about the potential for using fMRI-based functional connectomes in the development of biomarkers for autism spectrum disorder (ASD), the literature is full of negative findings-failures to distinguish ASD functional connectomes from those of typically developing controls (TD)-and positive findings that are inconsistent across studies. Here, we report on a new study designed to either better differentiate ASD from TD functional connectomes-or, alternatively, to refine our understanding of the factors underlying the current state of affairs. We scanned individuals with ASD and controls both at rest and while watching videos with social content. Using multiband fMRI across repeat sessions, we improved both data quantity and scanning duration by collecting up to 2 hr of data per individual. This is about 50 times the typical number of temporal samples per individual in ASD fcMRI studies. We obtained functional connectomes that were discriminable, allowing for near-perfect individual identification regardless of diagnosis, and equally reliable in both groups. However, contrary to what one might expect, we did not consistently or robustly observe in the ASD group either reductions in similarity to TD functional connectivity (FC) patterns or shared atypical FC patterns. Accordingly, FC-based predictions of diagnosis group achieved accuracy levels around chance. However, using the same approaches to predict scan type (rest vs. video) achieved near-perfect accuracy. Our findings suggest that neither the limitations of resting state as a "task," data resolution, data quantity, or scan duration can be considered solely responsible for failures to differentiate ASD from TD functional connectomes.
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http://dx.doi.org/10.1002/hbm.24943 | DOI Listing |
Psychiatry Clin Neurosci
January 2025
Department of Radiology, and Functional and Molecular Imaging key Laboratory of Sichuan Province, West China Hospital of Sichuan University, Chengdu, China.
Aim: As a central component of schizophrenia psychopathology, negative symptoms result in detrimental effects on long-term functional prognosis. However, the neurobiological mechanism underlying negative symptoms remains poorly understood, which limits the development of novel treatment interventions. This study aimed to identify the specific neural fingerprints of negative symptoms in schizophrenia.
View Article and Find Full Text PDFHum Brain Mapp
January 2025
Instituto de Neurobiología, Universidad Nacional Autónoma de México, Querétaro, Mexico.
Premature infants, born before 37 weeks of gestation can have alterations in neurodevelopment and cognition, even when no anatomical lesions are evident. Resting-state functional neuroimaging of naturally sleeping babies has shown altered connectivity patterns, but there is limited evidence on the developmental trajectories of functional organization in preterm neonates. By using a large dataset from the developing Human Connectome Project, we explored the differences in graph theory properties between at-term (n = 332) and preterm (n = 115) neonates at term-equivalent age, considering the age subgroups proposed by the World Health Organization for premature birth.
View Article and Find Full Text PDFNeurobiol Dis
January 2025
Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, China; National Clinical Research Center for Geriatric Disorders, Xuanwu Hospital, Capital Medical University, Beijing, China. Electronic address:
Background: Investigating brain metabolic networks is crucial for understanding the pathogenesis and functional alterations in Creutzfeldt-Jakob disease (CJD). However, studies on presymptomatic individuals remain limited. This study aimed to examine metabolic network topology reconfiguration in asymptomatic carriers of the PRNP G114V mutation.
View Article and Find Full Text PDFJ Neurol
January 2025
NMR Research Unit, Queen Square MS Centre, Department of Neuroinflammation, Faculty of Brain Sciences, UCL Queen Square Institute of Neurology, University College London, Queen Square, London, WC1N 3BG, UK.
Cognitive impairment (CI) in multiple sclerosis (MS) is only partially explained by whole-brain volume measures, but independent component analysis (ICA) can extract regional patterns of damage in grey matter (GM) or white matter (WM) that have proven more closely associated with CI. Pathology in GM and WM occurs in parallel, and so patterns can span both. This study assessed whether joint-ICA of GM and WM features better explained cognitive function compared to single-tissue ICA.
View Article and Find Full Text PDFJ Psychiatry Neurosci
January 2025
From the Department of Psychiatry, Yale University School of Medicine, New Haven, Conn., USA (Chen, Luo, Ide, C.-S. Li); Yale University, New Haven, Conn., USA (H.-T. Li); the Department of Biomedical Engineering, College of Chemistry and Life Science, Beijing University of Technology, Beijing, China (G. Li); the Beijing International Science and Technology Cooperation Base for Intelligent Physiological Measurement and Clinical Transformation, Beijing, China (G. Li); the Department of Neuroscience, Yale University School of Medicine, New Haven, Conn., USA (C.-S Li); the Interdepartment Neuroscience Program, Yale University, New Haven, Conn., USA (C.-S. Li); the Wu Tsai Institute, Yale University, New Haven, Conn., USA (C.-S. Li).
Background: Genetic variants may confer risk for depression by modulating brain structure and function; evidence has underscored the key role of the subgenual anterior cingulate cortex (sgACC) in depression. We sought to examine how the resting-state functional connectivity (rsFC) of the sgACC was associated with polygenic risk for depression in a subclinical population.
Methods: Following published protocols, we computed seed-based whole-brain sgACC rsFC and calculated polygenic risk scores (PRS) using data from healthy young adults from the Human Connectome Project.
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