ME/CFS is a complex disease with poorly understood immune dysregulation. Researchers used single-cell RNA sequencing to examine immune cells in patients and control cohorts. They found classical monocyte dysregulation in patients, suggesting inappropriate differentiation and migration. The study also identified patterns of improper platelet activation in patients, indicating immunological defects at baseline.
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Post-viral fatigue syndrome (PVFS) is a complex neuroimmune disorder characterized by disabling fatigue, joint pain, cognitive impairments, sleep disturbances, autonomic dysfunction, and neuropsychiatric symptoms. There are no definitive clinical criteria or FDA-approved therapies for PVFS. Mitochondria, crucial for tissue energy production, have been linked to low-grade systemic inflammation in conditions like ME/CFS, FM, and long COVID. This article reviews mitochondrial dysfunction in PVFS and evaluates coenzyme Q10 supplementation as a potential therapeutic strategy.
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ME/CFS is a complex disease with symptoms like fatigue, post-exertional malaise, and neurocognitive dysfunction. A study aimed to understand the relationship between immunological characteristics and intestinal barrier function in ME/CFS patients. Results showed reduced complement protein C4a levels in immunodeficient patients, suggesting innate immune dysregulation, and mucosal barrier leakage in those without immunodeficiency. This highlights the need for precise patient stratification and research to define effective treatment strategies.
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The study suggests that 5-hydroxytryptamine (5-HT) hyperactivation is linked to the pathogenic causes of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). Experimentally, high-dose serotonin reuptake inhibitor treatment led to severe fatigue and ME/CFS-associated symptoms in mice. The findings support the role of 5-HTergic hyperactivity in ME/CFS pathophysiology, providing valuable insights for understanding its biology and therapeutic approaches.
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Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a chronic condition with no identified diagnostic biomarkers. A study investigates the potential of inflammatome, immunome, and receptor-based biomarkers for evaluating ME/CFS progression. A dataset of 188 individuals was used, with a focus on severe cases. Results showed a stronger association between inflammatome and immunome markers in the severe group. Principal component factoring separated components associated with inflammatome, immunome, and receptor biomarkers. Random forest modeling showed excellent accuracy for splitting healthy/with condition groups and healthy/severity groups. The association between inflammatome and immunome markers is a candidate for controlled clinical study of ME/CFS progression markers, potentially aiding in treatment individualization.
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Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating illness with symptoms like fatigue, rhinitis, dry eyes, and sore throat. Mucin proteins, responsible for mucosal membrane formation, may contribute to ME/CFS symptoms due to inability to form adequate layers, particularly in the ocular and otolaryngological pathways, leading to chronic inflammation and exacerbation.
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Myalgic Encephalomyelitis/Cronic Fatigue Syndrome (ME/CFS) is a multisystem disease with unknown mechanisms. Circulating microRNAs (miRNA) are a promising candidate for endocrine mediators. A computational study reveals that aberrant miRNAs in ME/CFS target the same specific set of genes, which are functionally related. This leads to impairments in exercise hyperemia, angiogenic adaptations to hypoxia, antioxidant defenses, TGF-β signaling, and a shift towards mitochondrial fission. Transcription factors and epigenetic modulators are implicated, with uncertain downstream effects. The study suggests a central role for circulating microRNAs in ME/CFS etiology.
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