Chronic Fatigue Syndrome and DNA Hypomethylation of the Glucocorticoid Receptor Gene Promoter 1F Region

Vangeel, Elise; Eede, Filip Van Den; Hompes, Titia; Izzi, Benedetta; Favero, Jurgen Del; Moorkens, Greta; Lambrechts, Diether; Freson, Kathleen; Claes, Stephan

doi:10.1097/psy.0000000000000224

Cited by 42 publications

(54 citation statements)

References 44 publications

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“…In a study of 95 women from Belgium (Vangeel et al, 2015), mean and CpG site-specific NR3C1 1F promoter hypomethylation was seen in those with chronic fatigue syndrome (CFS; clinically diagnosed according to U.S. CDC criteria [Fukuda et al, 1994]) compared with healthy controls. In a study of 30 Chinese patients (Chen et al, 2015), there were significantly higher mean methylation levels across four NR3C1 first exon promoters (1D, 1E, 1F, and 1H) between systemic lupus erythematosus (SLE; clinically diagnosed according to American College of Rheumatology revised criteria [Hochberg, 1997]) and healthy control patients, but no results were reported for each of the individual promoters.…”

Section: Resultsmentioning

confidence: 99%

Epigenetic Pathways in Human Disease: The Impact of DNA Methylation on Stress-Related Pathogenesis and Current Challenges in Biomarker Development

et al. 2017

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HPA axis genes implicated in glucocorticoid regulation play an important role in regulating the physiological impact of social and environmental stress, and have become a focal point for investigating the role of glucocorticoid regulation in the etiology of disease. We conducted a systematic review to critically assess the full range of clinical associations that have been reported in relation to DNA methylation of CRH, CRH-R1/2, CRH-BP, AVP, POMC, ACTH, ACTH-R, NR3C1, FKBP5, and HSD11β1/2 genes in adults. A total of 32 studies were identified. There is prospective evidence for an association between HSD11β2 methylation and hypertension, and functional evidence of an association between NR3C1 methylation and both small cell lung cancer (SCLC) and breast cancer. Strong associations have been reported between FKBP5 and NR3C1 methylation and PTSD, and biologically-plausible associations have been reported between FKBP5 methylation and Alzheimer's Disease. Mixed associations between NR3C1 methylation and mental health outcomes have been reported according to different social and environmental exposures, and according to varying gene regions investigated. We conclude by highlighting key challenges and future research directions that will need to be addressed in order to develop both clinically meaningful prognostic biomarkers and an evidence base that can inform public policy practice.

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Section: Resultsmentioning

confidence: 99%

Epigenetic Pathways in Human Disease: The Impact of DNA Methylation on Stress-Related Pathogenesis and Current Challenges in Biomarker Development

et al. 2017

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“…Neurological biomarker studies (n = 4) focused on neurotransmitter regulation, but excluded imaging and functional studies [23–26]. The papers which could be retrieved for potential metabolic markers (n = 15) studied mitochondrial dysfunction, oxidative stress, cortisol regulation, and more comprehensive metabolic pathways [27–41]. …”

Section: The Euromene Me/cfs Biomarker Landscape Projectmentioning

confidence: 99%

The European ME/CFS Biomarker Landscape project: an initiative of the European network EUROMENE

et al. 2017

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Myalgic encephalomyelitis or chronic fatigue syndrome (ME/CFS) is a common and severe disease with a considerable social and economic impact. So far, the etiology is not known, and neither a diagnostic marker nor licensed treatments are available yet. The EUROMENE network of European researchers and clinicians aims to promote cooperation and advance research on ME/CFS. To improve diagnosis and facilitate the analysis of clinical trials surrogate markers are urgently needed. As a first step for developing such biomarkers for clinical use a database of active biomarker research in Europe was established called the ME/CFS EUROMENE Biomarker Landscape project and the results are presented in this review. Further we suggest strategies to improve biomarker development and encourage researchers to take these into consideration for designing and reporting biomarker studies.

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“…There is also evidence of abnormalities in the epigenetic regulation of gene expression in CFS patients diagnosed via narrow criteria, most notably in gene promoter methylation patterns and elevation of microRNAs (miRNAs) involved in the regulation of the immune system (Brenu et al 2014a; de Vega et al 2014, 2017; Petty et al 2016; Vangeel et al 2015, 2018). The work of de Vega and others is of particular interest as these authors also selected patients according to criteria mandating the presence of post-exertional malaise and examined global patterns of gene methylation rather than a single gene as was the case for Vangeel and colleagues (de Vega et al 2014, 2017; Vangeel et al 2015, 2018).…”

Section: Introductionmentioning

confidence: 99%

Myalgic encephalomyelitis or chronic fatigue syndrome: how could the illness develop?

et al. 2019

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A model of the development and progression of chronic fatigue syndrome (myalgic encephalomyelitis), the aetiology of which is currently unknown, is put forward, starting with a consideration of the post-infection role of damage-associated molecular patterns and the development of chronic inflammatory, oxidative and nitrosative stress in genetically predisposed individuals. The consequences are detailed, including the role of increased intestinal permeability and the translocation of commensal antigens into the circulation, and the development of dysautonomia, neuroinflammation, and neurocognitive and neuroimaging abnormalities. Increasing levels of such stress and the switch to immune and metabolic downregulation are detailed next in relation to the advent of hypernitrosylation, impaired mitochondrial performance, immune suppression, cellular hibernation, endotoxin tolerance and sirtuin 1 activation. The role of chronic stress and the development of endotoxin tolerance via indoleamine 2,3-dioxygenase upregulation and the characteristics of neutrophils, monocytes, macrophages and T cells, including regulatory T cells, in endotoxin tolerance are detailed next. Finally, it is shown how the immune and metabolic abnormalities of chronic fatigue syndrome can be explained by endotoxin tolerance, thus completing the model.

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Chronic Fatigue Syndrome and DNA Hypomethylation of the Glucocorticoid Receptor Gene Promoter 1F Region

Cited by 42 publications

References 44 publications

Epigenetic Pathways in Human Disease: The Impact of DNA Methylation on Stress-Related Pathogenesis and Current Challenges in Biomarker Development

Epigenetic Pathways in Human Disease: The Impact of DNA Methylation on Stress-Related Pathogenesis and Current Challenges in Biomarker Development

The European ME/CFS Biomarker Landscape project: an initiative of the European network EUROMENE

Myalgic encephalomyelitis or chronic fatigue syndrome: how could the illness develop?

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