scholarly journals DNA Methylation and Brain‐Derived Neurotrophic Factor Expression Account for Symptoms and Widespread Hyperalgesia in Patients With Chronic Fatigue Syndrome and Comorbid Fibromyalgia

2020 ◽  
Vol 72 (11) ◽  
pp. 1936-1944 ◽  
Author(s):  
Andrea Polli ◽  
Manosij Ghosh ◽  
Jelena Bakusic ◽  
Kelly Ickmans ◽  
Dora Monteyne ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Chronic Fatigue Syndrome ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Chronic Fatigue ◽  
Fatigue Syndrome ◽  
Factor Expression

Brain-derived neurotrophic factor concentration may not be depressed in chronic fatigue syndrome

2015 ◽  
Vol 3 (2) ◽  
pp. 122-125 ◽  
Author(s):  
David M. Patrick ◽  
Ruth R. Miller ◽  
Theodore Steiner ◽  
Jennifer L. Gardy ◽  
Shoshana M. Parker ◽  
...  
Keyword(s):  
Chronic Fatigue Syndrome ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Chronic Fatigue ◽  
Fatigue Syndrome ◽  
Factor Concentration

Integration of DNA methylation & health scores identifies subtypes in myalgic encephalomyelitis/chronic fatigue syndrome

Epigenomics ◽  
2018 ◽  
Vol 10 (5) ◽  
pp. 539-557 ◽  
Author(s):  
Wilfred C de Vega ◽  
Lauren Erdman ◽  
Suzanne D Vernon ◽  
Anna Goldenberg ◽  
Patrick O McGowan
Keyword(s):  
Dna Methylation ◽  
Chronic Fatigue Syndrome ◽  
Chronic Fatigue ◽  
Myalgic Encephalomyelitis ◽  
Fatigue Syndrome

scholarly journals Glucocorticoid receptor DNA methylation and childhood trauma in chronic fatigue syndrome patients

2018 ◽  
Vol 104 ◽  
pp. 55-60 ◽  
Author(s):  
Elise Beau Vangeel ◽  
Stefan Kempke ◽  
Jelena Bakusic ◽  
Lode Godderis ◽  
Patrick Luyten ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Chronic Fatigue Syndrome ◽  
Glucocorticoid Receptor ◽  
Childhood Trauma ◽  
Chronic Fatigue ◽  
Fatigue Syndrome

scholarly journals Identification of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome-associated DNA methylation patterns

PLoS ONE ◽  
2018 ◽  
Vol 13 (7) ◽  
pp. e0201066 ◽  
Author(s):  
Malav S. Trivedi ◽  
Elisa Oltra ◽  
Leonor Sarria ◽  
Natasha Rose ◽  
Vladimir Beljanski ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Chronic Fatigue Syndrome ◽  
Chronic Fatigue ◽  
Myalgic Encephalomyelitis ◽  
Fatigue Syndrome ◽  
Methylation Patterns

scholarly journals Brain derived neurotrophic factor expression and DNA methylation in response to subchronic valproic acid and/or aldosterone treatment

2019 ◽  
Vol 60 (2) ◽  
pp. 71-77
Author(s):  
Katarina Buzgoova ◽  
Jan Graban ◽  
Lucia Balagova ◽  
Natasa Hlavacova ◽  
Daniela Jezova
Keyword(s):  
Dna Methylation ◽  
Valproic Acid ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Factor Expression

scholarly journals DNA Methylation Modifications Associated with Chronic Fatigue Syndrome

PLoS ONE ◽  
2014 ◽  
Vol 9 (8) ◽  
pp. e104757 ◽  
Author(s):  
Wilfred C. de Vega ◽  
Suzanne D. Vernon ◽  
Patrick O. McGowan
Keyword(s):  
Dna Methylation ◽  
Chronic Fatigue Syndrome ◽  
Chronic Fatigue ◽  
Fatigue Syndrome

scholarly journals A Cartography of Differential Gene Methylation in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Different Network Roles in the Protein-Protein Interactions Network Play Different, Biologically Relevant, Roles

2021 ◽  
Author(s):  
Aurelia Wilberforce ◽  
Giulio Valentino Dalla Riva
Keyword(s):  
Dna Methylation ◽  
Chronic Fatigue Syndrome ◽  
Sample Size ◽  
Protein Interactions ◽  
Small Sample Size ◽  
Chronic Fatigue ◽  
Small Sample ◽  
Myalgic Encephalomyelitis ◽  
Fatigue Syndrome ◽  
Differentially Methylated Genes

Myalgic Encephalomyelitis, also known as Chronic Fatigue Syndrome (ME/CFS), is a debilitating illness characterised by severe fatigue and associated with immune dysfunction. Previous studies of DNA methylation (epigenetic changes that can affect the gene transcription) have found evidence of changes in immune cells for ME/CFS. However these studies have been limited by their small sample size, precluding the ability to detect changes to methylation of smaller magnitude. Therefore, to achieve a larger sample size and detect small changes to DNA methylation, we aggregate three comparable datasets and analyse them in unison. We find 10,824 differentially methylated genes, with a very small average change. We then turn our attention to the network structure of the Protein-Protein interaction, which we built from the currently known interactions of relevant proteins, and localising the network cartography framework, we identify 184 hub genes. A distinct structuring emerges, with different hub types playing differing, meaningful, biological roles. Supporting previous theories about ME/CFS, Gene ontology enrichment analysis of these hubs reveal that they are involved in immune system processes, including response to TGF-β and LPS, as well as mitochondrial functioning. We also show that dopaminergic signalling may potentially contribute to immune pathology in ME/CFS. Our results demonstrate the potentiality of network cartographic approaches in shedding light on the epigenetic contribution to the immune dysregulation of ME/CFS.

scholarly journals Changes in DNA methylation profiles of myalgic encephalomyelitis/chronic fatigue syndrome patients reflect systemic dysfunctions

2020 ◽  
Vol 12 (1) ◽  
Author(s):  
A. M. Helliwell ◽  
E. C. Sweetman ◽  
P. A. Stockwell ◽  
C. D. Edgar ◽  
A. Chatterjee ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Chronic Fatigue Syndrome ◽  
Chronic Fatigue ◽  
Myalgic Encephalomyelitis ◽  
Pathway Enrichment Analysis ◽  
Healthy Controls ◽  
Sequencing Data ◽  
Peripheral Blood Mononuclear ◽  
Fatigue Syndrome ◽  
Array Technology

Abstract Background Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a lifelong debilitating disease with a complex pathology not yet clearly defined. Susceptibility to ME/CFS involves genetic predisposition and exposure to environmental factors, suggesting an epigenetic association. Epigenetic studies with other ME/CFS cohorts have used array-based technology to identify differentially methylated individual sites. Changes in RNA quantities and protein abundance have been documented in our previous investigations with the same ME/CFS cohort used for this study. Results DNA from a well-characterised New Zealand cohort of 10 ME/CFS patients and 10 age-/sex-matched healthy controls was isolated from peripheral blood mononuclear (PBMC) cells, and used to generate reduced genome-scale DNA methylation maps using reduced representation bisulphite sequencing (RRBS). The sequencing data were analysed utilising the DMAP analysis pipeline to identify differentially methylated fragments, and the MethylKit pipeline was used to quantify methylation differences at individual CpG sites. DMAP identified 76 differentially methylated fragments and Methylkit identified 394 differentially methylated cytosines that included both hyper- and hypo-methylation. Four clusters were identified where differentially methylated DNA fragments overlapped with or were within close proximity to multiple differentially methylated individual cytosines. These clusters identified regulatory regions for 17 protein encoding genes related to metabolic and immune activity. Analysis of differentially methylated gene bodies (exons/introns) identified 122 unique genes. Comparison with other studies on PBMCs from ME/CFS patients and controls with array technology showed 59% of the genes identified in this study were also found in one or more of these studies. Functional pathway enrichment analysis identified 30 associated pathways. These included immune, metabolic and neurological-related functions differentially regulated in ME/CFS patients compared to the matched healthy controls. Conclusions Major differences were identified in the DNA methylation patterns of ME/CFS patients that clearly distinguished them from the healthy controls. Over half found in gene bodies with RRBS in this study had been identified in other ME/CFS studies using the same cells but with array technology. Within the enriched functional immune, metabolic and neurological pathways, a number of enriched neurotransmitter and neuropeptide reactome pathways highlighted a disturbed neurological pathophysiology within the patient group.

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