Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease Presenting as Intracranial Hypertension

Chaudhuri, Jaydip Ray; Bagul, Jui Jade; Alluri, Swathi; Singhal, Bhim; Reddy, N. Chakradhar; Vallam, Kiran Kumar

doi:10.1212/nxi.0000000000200020

Cited by 12 publications

(4 citation statements)

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“…Signaling pathways include signaling by GPCR [56] and extracellular matrix organization [57] were responsible for advancement of HD. Research has shown that CBLN2 [58], MOG (myelin oligodendrocyte glycoprotein) [59], ROS1 [60], LGR6 [61], GJA5 [62], SUCNR1 [63], REN (renin) [64], VEGFC (vascular endothelial growth factor C) [65], TLR2 [66], FGF12 [67], WT1 [68], SLC22A3 [69], CSRP3 [70], PAPPA2 [71], ACAN (aggrecan) [72], SHH (sonic hedgehog signaling molecule) [73], PDC (phosducin) [74], AGTR1 [75], XDH (xanthine dehydrogenase) [76], P2RX7 [77], NTSR1 [78], SIRT2 [79], RBP4 [80], BMP2 [81], ERBB3 [82], HAS2 [83], CDH13 [84], CSMD1 [85], NR3C2 [86], EPAS1 [87], TRPC6 [88], MMP3 [89], ERAP2 [90], HLA-DRB1 [91], CD74 [92], VWF (von Willebrand factor) [93], MTTP (microsomal triglyceride transfer protein) [494], ANGPT2 [184], AKR1C3 [495], NEDD4L [496], CASP1 [497], LDB2 [498], CHRNA5 [499], CCND2 [500], BRCA2 [97], ZBTB20 [501], EFNB2 [502], CYP7B1 [503], DCLK1 [504], RBM20 [505], PLCE1 [197], protein) [94], NEDD4L [95], CASP1 [96], BRCA2 [97], EFNB2 [98], PLCE1 [99], EGFR (epidermal growth factor receptor) [100], ABCA1 [101], CRHR2 [102], RND3 [103], COMT (catechol-O-methyltransferase) [104] and SMAD9 [105] plays an important role in the pathogenesis of hypertension. Studies have revealed that NEUROD4 [106], SOX10 [107], MOG (myelin oligodendrocyte glycoprotein) [108], NR5A2 [109], GLRA3 [110], FA2H [111], SERPINA […”

Section: Discussionmentioning

confidence: 99%

Identification of key genes and signaling pathway in the pathogenesis of Huntington's disease via bioinformatics and next generation sequencing data analysis

Vastrad,

Vastrad

2024

Preprint

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Huntington's disease (HD) is the primary cause of progressive motor deficits, psychiatric symptoms, and cognitive impairment. The exact molecular mechanisms of HD pathogenesis are largely unknown. This investigation aims to identify the hub genes, miRNA and TFs in HD and explore their potential molecular regulatory network. Next generation sequencing (NGS) dataset (GSE105041) was extracted from the Gene Expression Omnibus (GEO) database. An integrated bioinformatics pipeline including identification of differentially expressed genes (DEGs), Gene ontology and REACTOME pathway enrichment analysis, protein-protein interaction (PPI) network and module analysis, miRNA-hub gene regulatory network analysis and TF-hub gene regulatory network analysis, and receiver operating characteristic curve (ROC) analysis were applied to identify hub genes, miRNA and TFs, and key drivers of HD pathogenesis. We identified 958 DEGs in the discovery phase, consisting of 479 up regulated genes and 479 down regulated genes. GO and REACTOME enrichment analyses of the 479 up regulated genes and 479 down regulated genes showed that they were mainly involved in multicellular organismal process, developmental process, signaling by GPCR and MHC class II antigen presentation. Further analysis of the PPI network using Cytoscape and PEWCC plugins identified 10 hub genes, including LRRK2, MTUS2, HOXA1, IL7R, ERBB3, EGFR, TEX101, WDR76, NEDD4L and COMT. Possible target miRNAs and TFs, including hsa-mir-1292-5p, hsa-mir-4521, ESRRB and SREBF1, were predicted by constructing a miRNA-hub gene regulatory network analysis and TF-hub gene regulatory network. This investigation used bioinformatics methods to explore the molecular pathogenesis of HD, and identified potential molecular markers. These molecular markers might provide novel ideas and methods for the early diagnosis, treatment, and monitoring of HD.

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Section: Discussionmentioning

confidence: 99%

Identification of key genes and signaling pathway in the pathogenesis of Huntington's disease via bioinformatics and next generation sequencing data analysis

Vastrad,

Vastrad

2024

Preprint

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“…Increased cerebrospinal fluid (CSF) in the inflammatory context is more commonly associated with manifestations such as acute disseminated encephalomyelitis or meningoencephalitis [15]. One previously reported potential cause of increased CSF production in MOGAD without evidence of encephalitis might involve low-grade meningeal inflammation producing increased CSF [15].…”

Section: Discussionmentioning

confidence: 99%

Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease: A Case Report

Teru,

Dogiparthi,

Bonitz

et al. 2024

Cureus

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Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a newly discovered autoimmune demyelinating disorder. The clinical manifestations of MOGAD are divergent but often characterized by inflammatory central nervous system (CNS) deficits such as optic neuritis, encephalitis, or transverse myelitis that predominantly affect the pediatric population. Despite the distinct features often associated with MOGAD, the disease exhibits a diverse range of clinical manifestations, making timely diagnosis and treatment challenging. In particular, distinguishing MOGAD from multiple sclerosis (MS) is important for adequate treatment and the prevention of relapsing disease. In this report, we present a rare case of MOGAD in a 57-year-old male who initially exhibited symptoms of bilateral optic nerve edema and flame hemorrhage. This led to an initial misdiagnosis of pseudotumor cerebri. Serological analysis at a tertiary care center ultimately led to the diagnosis of MOGAD after multiple visits to the ophthalmologist with worsening vision deficits.

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“…Clinically it associated fever, headaches, vomiting and possible meningeal irritation signs [46]. Evaluation of CSF is characterized by pleocytosis and elevated cranial pressure [47]. By definition, the complete work-up for infectious aetiology is negative.…”

Section: Core Clinical Demyelinating Events: Classical Features and R...mentioning

confidence: 99%

Clinical characteristics of patients with myelin oligodendrocyte glycoprotein antibodies

Maillart,

Deiva,

Marignier

2024

Current Opinion in Neurology

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Purpose of review The clinical landscape associated to myelin oligodendrocyte glycoprotein antibodies (MOG-Ab) has undergone a remarkable transformation over the past two decades, primarily driven by advancements in antibody detection techniques that have enhanced both the specificity and sensitivity of assays, enabling the identification of novel clinical phenotypes. Recent findings Recent pivotal research publications, comprehensive reviews from established research groups, and most notably the first proposed international criteria for MOG-Ab associated disease (MOGAD) have substantially enriched our understanding of the clinical features associated with MOG-Ab. This review presents a comprehensive overview of the clinical characteristics of patients with MOG-Ab, systematically examining each core clinical syndrome defined by the proposed international MOGAD criteria. We incorporated recent insights and discussed potential challenges in applying these criteria across diverse clinical scenarios. Summary The proposed international MOGAD criteria provide a comprehensive, homogeneous, and specific framework for characterizing the clinical features of patients with MOG-Ab, encompassing both paediatric and adult populations. In the future, the widespread adoption of specific and reliable assays for MOG-Ab detection, complemented by the development of surrogate fluid and imaging markers, holds promise for better characterizing atypical presentations, only-cerebrospinal fluid positivity and the MOGAD “seronegative” situations.

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Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease Presenting as Intracranial Hypertension

Cited by 12 publications

References 12 publications

Identification of key genes and signaling pathway in the pathogenesis of Huntington's disease via bioinformatics and next generation sequencing data analysis

Identification of key genes and signaling pathway in the pathogenesis of Huntington's disease via bioinformatics and next generation sequencing data analysis

Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease: A Case Report

Clinical characteristics of patients with myelin oligodendrocyte glycoprotein antibodies

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