• World Neurosurg · Aug 2024

    Disulfidoptosis as a Novel Mechanism of Neuronal Death: Insights from Creutzfeldt-Jakob Disease.

    • Qike Wu, Shan-Peng Liu, Cuiying Liu, Xiaoyuan Chen, Hongmei Zhou, and Heng Zhao.
    • Beijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Joint Innovation Center for Brain Disorders, Capital Medical University, Beijing, China.
    • World Neurosurg. 2024 Aug 17.

    BackgroundSporadic Creutzfeldt-Jakob Disease (SCJD) is a severe neurodegenerative disorder characterized by rapid progression and extensive neuronal loss. Disulfidptosis is an innovative type of programmed cell demise characterized by an accumulation of disulfide bonds within the cellular cytoplasm, subsequently triggering functional disruption and cell demise.MethodsThrough literature review and analysis, we identified 18 candidate disulfidptosis-related genes (DRGs) involved in cellular processes. The dataset used for analysis, GSE124571, was obtained from the Gene Expression Omnibus database. Gene-gene and protein-protein interactions were analyzed using the GeneMANIA and STRING databases, respectively. We also performed enrichment analysis, differential expressed genes analysis, weighted gene correlation network analysis analysis, immune infiltration, consensus clustering, and matrix correlation.ResultsThe analysis showed that 12 out of 18 DRGs were significantly changed between SCJD and control groups. The DRGs had strong interactions such as physical interactions, co-expression and genetic interactions, and were enriched in biological processes and pathways related to actin cytoskeletal regulation. The study most notably identified 3 hub genes (WASF2, TLN1 and G6PD) important for SCJD and emphasized the functional significance of the identified hub genes. The role of the immune system in the pathogenesis of SCJD. The study found that the composition of immune cells in SCJD brain tissue is altered. Consensus clustering provided insights into immune infiltration and hub gene expression in SCJD subgroup.ConclusionsOur study reveals the possible involvement of disulfidptosis in SCJD and highlights the significance of identified hub genes as potential biomarkers and therapeutic targets for SCJD.Copyright © 2024 Elsevier Inc. All rights reserved.

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