A bibliometric analysis of neuroimaging studies on cognitive control in autism spectrum disorder (2000–2025)

ObjectiveThis study aims to systematically analyze neuroimaging research on cognitive control in Autism spectrum disorder (ASD) from 2000 to 2025 using bibliometric methods, in order to reveal the evolutionary trajectory, core knowledge base, research hotspots, and future frontiers of the field.MethodsA search was conducted on the Web of Science Core Collection and Scopus databases, resulting in the inclusion of 1,581 relevant articles. VOSviewer and the Bibliometrix package in R were utilized to conduct a comprehensive visualization and quantitative analysis of annual publication volume, country/institution/author collaboration networks, keyword co-occurrence, document co-citation, and thematic evolution.Results(1) The volume of research literature showed exponential growth, with an annual growth rate of 21.61%, entering a period of rapid development particularly after 2012, which is closely related to the popularization of functional magnetic resonance imaging (fMRI) technology. (2) “Functional connectivity,” “executive function,” and “default mode network” were the most central keywords. “Functional connectivity” rapidly became a hub connecting various themes after 2010, marking a paradigm shift from “functional localization” to “brain network dysregulation.” (3) The “Triple network model” proposed by Menon was the most cited document, laying the core theoretical foundation for understanding ASD as a disorder of large-scale brain network dysfunction. (4) “Transdiagnostic” research has emerged as a new hotspot, while “multimodal imaging,” “machine learning,” and “dynamic connectivity” represent highly promising future directions.ConclusionOver the past two decades, neuroimaging research on cognitive control in ASD has undergone a profound paradigm shift: from focusing on abnormal activation in isolated brain regions to exploring the static and dynamic dysregulation of large-scale brain networks. The research perspective has also expanded from a single-disorder model to a transdiagnostic framework that includes comparisons with other neurodevelopmental disorders (e.g., ADHD). Future research should focus on the fusion of multimodal data, the application of computational psychiatry methods, and the translation of basic research findings into personalized clinical interventions.

A framework for building a synthetic cell from the SynCell Asia Initiative

Nature Biotechnology, Published online: 26 May 2026; doi:10.1038/s41587-026-03153-w

Building a living cell from scratch requires overcoming a bottleneck that has remained unresolved despite decades of progress: orchestrating the spatiotemporal integration of core functional modules. To tackle this barrier, the SynCell Asia Initiative outlines a strategy for developing core functional modules followed by their systems-level integration through the establishment of a centralized, artificial intelligence (AI)-driven biofoundry.

Fibroblast growth factor receptor inhibition for succinate dehydrogenase-deficient gastrointestinal stromal tumors: a phase 2 trial

Nature Medicine, Published online: 26 May 2026; doi:10.1038/s41591-026-04376-9

In a multicenter phase 2 trial, the fibroblast growth factor receptor inhibitor rogaratinib showed encouraging clinical efficacy in patients with succinate dehydrogenase-deficient gastrointestinal stromal tumors, suggesting a potential new treatment option for this patient population and demonstrating that an epigenetic mechanism of oncogene activation can be successfully targeted with a tyrosine kinase inhibitor.

Microglial mitochondria transfer to astrocytes via GPNMB-enriched extracellular vesicles alleviates cognitive deficits in tauopathy mice

Nature Neuroscience, Published online: 26 May 2026; doi:10.1038/s41593-026-02317-w

In PS19 mice, microglia-derived glycoprotein nonmetastatic melanoma protein B promotes mitochondrial extracellular vesicle secretion, enabling mitochondrial transfer to astrocytes. This improves astrocytic function and reduces Alzheimer’s disease (AD) symptoms, while GPNMB deficiency impairs it, highlighting new AD treatment avenues.