Charlotte Stephens, Research Correspondent, ME Association.
We show below brief summaries of the research studies about ME/CFS that have been published in the last week, followed by the abstracts from those studies.
All research relating to ME/CFS can be located in the ME Association: Index of ME/CFS Published Research.
This extensive library of research is updated at the end of every month, and is correct to the end of September 2020. It is a free resource available to anyone.
The Index provides an A-Z of published research studies and selected key documents and articles, listed by subject matter, on myalgic encephalomyelitis, myalgic encephalopathy, and/or chronic fatigue syndrome (ME/CFS).
You can use it to easily locate and read any research in a particular area that you might be interested in, e.g. epidemiology, infection, neurology, post-exertional malaise etc.
You can also find the Research Index in the Research section of the website together with a list of Research Summaries that provide lay explanations of the more important and interesting work that has been published to date.
ME/CFS Research Published 25 September – 01 October 2020
This week, 1 new research study has been published.
Researchers from New Zealand carried out a small study looking at proteins in a type of immune cell that were either raised or decreased in ME/CFS patients compared to controls.
They found 99 proteins to be different in ME/CFS patients, a proportion of which were involved in mitochondrial function. A significant number were also involved in previously implicated disturbances in ME/CFS, such as the immune inflammatory response.
The results of this study support other studies which have found deficient ATP production in ME/CFS, as well as increased inflammation.
ME/CFS Research References and Abstracts
1. Sweetman E et al. (2020)
A SWATH-MS analysis of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome peripheral blood mononuclear cell proteomes reveals mitochondrial dysfunction.
Journal of Translational Medicine 18 (365).
Background: Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a serious and complex physical illness that affects all body systems with a multiplicity of symptoms, but key hallmarks of the disease are pervasive fatigue and ‘post-exertional malaise’, exacerbation after physical and/or mental activity of the intrinsic fatigue and other symptoms that can be highly debilitating and last from days to months.
Although the disease can vary widely between individuals, common symptoms also include pain, cognitive deficits, sleep dysfunction, as well as immune, neurological and autonomic symptoms.
Typically, it is a very isolating illness socially, carrying a stigma because of the lack of understanding of the cause and pathophysiology.
Methods: To gain insight into the pathophysiology of ME/CFS, we examined the proteomes of peripheral blood mononuclear cells (PBMCs) by SWATH-MS analysis in a small well-characterised group of patients and matched controls.
A principal component analysis (PCA) was used to stratify groups based on protein abundance patterns, which clearly segregated the majority of the ME/CFS patients (9/11) from the controls. This majority subgroup of ME/CFS patients was then further compared to the control group.
Results: A total of 60 proteins in the ME/CFS patients were differentially expressed (P < 0.01, Log10 (Fold Change) > 0.2 and < −0.2). Comparison of the PCA selected subgroup of ME/CFS patients (9/11) with controls increased the number of proteins differentially expressed to 99.
Of particular relevance to the core symptoms of fatigue and post-exertional malaise experienced in ME/CFS, a proportion of the identified proteins in the ME/CFS groups were involved in mitochondrial function, oxidative phosphorylation, electron transport chain complexes, and redox regulation.
A significant number were also involved in previously implicated disturbances in ME/CFS, such as the immune inflammatory response, DNA methylation, apoptosis and proteasome activation.
Conclusions: The results from this study support a model of deficient ATP production in ME/CFS, compensated for by upregulation of immediate pathways upstream of Complex V that would suggest an elevation of oxidative stress.
This study and others have found evidence of a distinct pathology in ME/CFS that holds promise for developing diagnostic biomarkers.
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