scholarly journals A Comparison of Neuroimaging Abnormalities in Multiple Sclerosis, Major Depression and Chronic Fatigue Syndrome (Myalgic Encephalomyelitis): is There a Common Cause?

2017 ◽  
Vol 55 (4) ◽  
pp. 3592-3609 ◽  
Author(s):  
Gerwyn Morris ◽  
Michael Berk ◽  
Basant K. Puri
Keyword(s):  
Multiple Sclerosis ◽  
Major Depression ◽  
Chronic Fatigue Syndrome ◽  
Chronic Fatigue ◽  
Myalgic Encephalomyelitis ◽  
Common Cause ◽  
Fatigue Syndrome

scholarly journals A Preliminary Comparative Assessment of the Role of CD8+ T Cells in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis and Multiple Sclerosis

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Ekua W. Brenu ◽  
Simon Broadley ◽  
Thao Nguyen ◽  
Samantha Johnston ◽  
Sandra Ramos ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
T Cells ◽  
Chronic Fatigue Syndrome ◽  
Cd8 T Cells ◽  
Preliminary Investigation ◽  
Chronic Fatigue ◽  
Myalgic Encephalomyelitis ◽  
Effector Memory ◽  
Fatigue Syndrome ◽  
The Status

Background. CD8+ T cells have putative roles in the regulation of adaptive immune responses during infection. The purpose of this paper is to compare the status of CD8+ T cells in Multiple Sclerosis (MS) and Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME).Methods. This preliminary investigation comprised 23 CFS/ME patients, 11 untreated MS patients, and 30 nonfatigued controls. Whole blood samples were collected from participants, stained with monoclonal antibodies, and analysed on the flow cytometer. Using the following CD markers, CD27 and CD45RA (CD45 exon isoform 4), CD8+ T cells were divided into naïve, central memory (CM), effector memory CD45RA− (EM), and effector memory CD45RA+ (EMRA) cells.Results. Surface expressions of BTLA, CD127, and CD49/CD29 were increased on subsets of CD8+ T cells from MS patients. In the CFS/ME patients CD127 was significantly decreased on all subsets of CD8+ T cells in comparison to the nonfatigued controls. PSGL-1 was significantly reduced in the CFS/ME patients in comparison to the nonfatigued controls.Conclusions. The results suggest significant deficits in the expression of receptors and adhesion molecules on subsets of CD8+ T cells in both MS and CFS/ME patients. These deficits reported may contribute to the pathogenesis of these diseases. However, larger sample size is warranted to confirm and support these encouraging preliminary findings.

scholarly journals Lymphocyte subset differences in patients with chronic fatigue syndrome, multiple sclerosis and major depression

2005 ◽  
Vol 141 (2) ◽  
pp. 326-332 ◽  
Author(s):  
M. J. Robertson ◽  
R. S. Schacterle ◽  
G. A. Mackin ◽  
S. N. Wilson ◽  
K. L. Bloomingdale ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Major Depression ◽  
Chronic Fatigue Syndrome ◽  
Chronic Fatigue ◽  
Lymphocyte Subset ◽  
Fatigue Syndrome

scholarly journals You + ME Registry: A Research Platform to Facilitate Clinical and Therapeutic Discoveries in ME/CFS and Related Diseases

2021 ◽  
Author(s):  
Allison Ramiller ◽  
Kathleen Mudie ◽  
Elle Seibert ◽  
Sadie Whittaker
Keyword(s):  
Multiple Sclerosis ◽  
Big Data ◽  
Chronic Fatigue Syndrome ◽  
Chronic Fatigue ◽  
Health Data ◽  
Myalgic Encephalomyelitis ◽  
Fatigue Syndrome ◽  
Research Platform ◽  
And Control

ME/CFS (Myalgic Encephalomyelitis / Chronic Fatigue Syndrome) is a chronic, complex, heterogeneous disease that affects millions and lacks both diagnostics and treatments. Big data, or the collection of vast quantities of data that can be mined for information, has transformed the understanding of many complex illnesses like cancer (1,2) and multiple sclerosis (3,4), by dissecting heterogeneity, identifying subtypes, and enabling the development of personalized treatments. It is possible that big data can reveal the same for ME/CFS. Solve M.E. developed and launched the You + ME Registry to collect longitudinal health data from people with ME/CFS, people with Long COVID (LC) and control volunteers using rigorous protocols designed to harmonize with other groups collecting data from similar groups of people. The Registry is an invaluable resource because it integrates with a symptom tracking app, as well as a biorepository, to provide a robust and rich dataset that is available to qualified researchers. Accordingly, it facilitates collaboration that may ultimately uncover causes and help accelerate the development of therapies.

Immunologic parameters in chronic fatigue syndrome, major depression, and multiple sclerosis

1998 ◽  
Vol 105 (3) ◽  
pp. 43S-49S ◽  
Author(s):  
Benjamin H Natelson ◽  
John J LaManca ◽  
Thomas N Denny ◽  
Adrian Vladutiu ◽  
James Oleske ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Major Depression ◽  
Chronic Fatigue Syndrome ◽  
Chronic Fatigue ◽  
Fatigue Syndrome ◽  
Immunologic Parameters

scholarly journals The UK ME/CFS Biobank for biomedical research on Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Multiple Sclerosis

2017 ◽  
Vol 4 ◽  
Author(s):  
Eliana M Lacerda ◽  
Erinna W Bowman ◽  
Jacqueline M Cliff ◽  
Caroline C Kingdon ◽  
Elizabeth C King ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Chronic Fatigue Syndrome ◽  
Biomedical Research ◽  
Chronic Fatigue ◽  
Myalgic Encephalomyelitis ◽  
Fatigue Syndrome ◽  
The Uk

scholarly journals Circulating levels of GDF15 in patients with myalgic encephalomyelitis/chronic fatigue syndrome

2019 ◽  
Vol 17 (1) ◽  
Author(s):  
A. Melvin ◽  
E. Lacerda ◽  
H. M. Dockrell ◽  
S. O’Rahilly ◽  
L. Nacul
Keyword(s):  
Multiple Sclerosis ◽  
Chronic Fatigue Syndrome ◽  
Cellular Stress ◽  
Chronic Fatigue ◽  
Myalgic Encephalomyelitis ◽  
Healthy Controls ◽  
Skeletal Muscle Fatigue ◽  
Fatigue Syndrome ◽  
The Brain ◽  
Circulating Levels

Abstract Background Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating condition characterised by fatigue and post-exertional malaise. Its pathogenesis is poorly understood. GDF15 is a circulating protein secreted by cells in response to a variety of stressors. The receptor for GDF15 is expressed in the brain, where its activation results in a range of responses. Among the conditions in which circulating GDF15 levels are highly elevated are mitochondrial disorders, where early skeletal muscle fatigue is a key symptom. We hypothesised that GDF15 may represent a marker of cellular stress in ME/CFS. Methods GDF15 was measured in serum from patients with ME/CFS (n = 150; 100 with mild/moderate and 50 with severe symptoms), “healthy volunteers” (n = 150) and a cohort of patients with multiple sclerosis (n = 50). Results Circulating GDF15 remained stable in a subset of ME/CFS patients when sampled on two occasions ~ 7 months (IQR 6.7–8.8) apart, 720 pg/ml (95% CI 625–816) vs 670 pg/ml (95% CI 598–796), P = 0.5. GDF15 levels were 491 pg/ml in controls (95% CI 429–553), 546 pg/ml (95% CI 478–614) in MS patients, 560 pg/ml (95% CI 502–617) in mild/moderate ME/CFS patients and 602 pg/ml (95% CI 531–674) in severely affected ME/CFS patients. Accounting for potential confounders, severely affected ME/CFS patients had GDF15 concentrations that were significantly increased compared to healthy controls (P = 0.01). GDF15 levels were positively correlated (P = 0.026) with fatigue scores in ME/CFS. Conclusions Severe ME/CFS is associated with increased levels of GDF15, a circulating biomarker of cellular stress that appears which stable over several months.

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