Research Projects
ME Association funded research on ME/CFS and Long Covid
Below is a list of research papers funded completely or partially by the ME Association, on myalgic encephalomyelitis, myalgic encephalopathy, and/or chronic fatigue syndrome (ME/CFS), and Long Covid.
Current Projects
Ramsay Biomedical Research Projects
MEA Grant: £131,919
University of British Columbia, Canada
Principal Investigator: Dr Luis Nacul
Start Date: 13/03/2025 (The start of MEA Funding. The trial was commissioned by CIHR in April 2021 but was delayed by the pandemic.)
Duration: 19 months
Status: In progress
MEA Grant: £76,989.50
Brunel University, London
Principal Investigators: Dr Jackie Cliff and Dr Fatima Labeed
Start Date: 01/08/2025
Duration: 24 months
Status: In progress
MEA Grant: £32,149.30
UK Dementia Research Institute’s Fluid Biomarker Laboratory at University College London (UCL)
Principal Investigator: Miss Sophie Hicks (Supervisors: Dr Amanda Heslegrave, Dr Michael Zandi, Professor Henrik Zetterberg)
Start Date: 01/12/2025
Duration: 12 months
Status: In progress
MEA Grant: £2,500 per PM (Max. 10 PMs per year)
Manchester Brain Bank, University of Manchester
Principal Investigator: Dr Andrew Robinson
Start Date: 19/10/2023
Status: In progress
MEA Grant: £16,971 (The UKRI is also providing a grant to the RFI)
Rosalind Franklin Institute (RFI), University of Oxford
Principal Investigator: Aleyna Lumsden (Supervisors: Dr Bela Paiza and Professor Karl Morten)
Start Date: 01/10/2025
Duration: 48 months
Status: In progress
MEA Grant: £39,554.13 (Phase 1)
Oxford Centre for Clinical Magnetic Resonance Research (OCMR), University of Oxford
Principal Investigator: Professor Ladislav Valkovič
Start Date: 01/04/2026
Duration: 12 months
Status: In progress
Ramsay Healthcare Research Projects
MEA Grant: £11,178.20
DePaul University, Chicago, USA
Principal Investigator: Professor Leonard Jason
Start Date: 15/09/2025
Duration: 24 months
Status: In progress
MEA Grant: £7,985
University of Liverpool
Principal Investigator: Karen Leslie (Supervisors: Dr Andrew King and Dr Nicola Baker)
Start Date: 01/07/2024
Duration: 72 months
Status: In progress
MEA Grant: £59,750
University of Manchester
Principal Investigator: Professor Sarah Tyson
Start Date: 01/08/2025
Duration: 18 months
Status: In progress
MEA Grant: £87,000
University of Manchester
Principal Investigator: Dr Keith Geraghty
Start Date: 13/01/2026
Duration: 18 months
Status: In progress
MEA Grant: £29,880
Newcastle University
Principal Investigator: Dr Mark Pearce
Start Date: subject to recruitment of new team membe)
Duration: 12 months
Status: On hold
Archive
- 2026: Leeds: Testing a Personalised Dysautonomia Management Protocol in Patients with Orthostatic Intolerance and a Diagnosis of ME/CFS or Long Covid: Sivan, M et al.
Conclusion: The results suggest that targeted conservative interventions could influence autonomic function and symptom reduction. However, the magnitude of change was limited, and statistical significance might not necessarily relate to a clinically significant improvement in symptoms. - 2026: Oxford: Hub for ME/CFS Research into Biological Understanding and Biomarker Research: Morten, K et al.
The Morten Group has been at the forefront of investigating the biological mechanisms of ME/CFS, with a particular focus on mitochondrial dysfunction, oxidative stress, and metabolic abnormalities. - 2025: Exeter: Understanding Symptom Clusters, Diagnosis and Healthcare Experiences in ME/CFS and Long Covid: A Cross-sectional Survey in the UK: Mansoubi, M et al.
Conclusion: ME/CFS and Long Covid share overlapping but distinct symptom clusters, indicating common challenges in management. The findings highlight significant delays in diagnosis and low satisfaction with specialist services, suggesting a need for improved self-management resources and better-coordinated care across the NHS. - 2025: Guildford: The Search for a Blood-based Biomarker for ME/CFS: from Biochemistry to Electrophysiology: Clarke, KSP et al.
Conclusion: Different biochemical and electrophysiological properties which differentiate ME/CFS have been identified across studies, holding promise as potential blood-based quantitative diagnostic biomarkers for ME/CFS. However, further research is required to determine their specificity to ME/CFS and adoptability for clinical use. - 2025: Oxford: Dysregulation of lipid metabolism, energy production, and oxidative stress in ME/CFS, GWS and FM: Davis, L et al.
Conclusion: The precise mechanisms driving altered metabolic pathways in ME/CFS, GWS, and FM remain to be elucidated; however, the elevated oxidative stress observed across these illnesses may contribute to symptoms and offer a potential target for therapeutic intervention. Investigating the mechanisms, and their role in the disease process, could provide insights into disease pathogenesis and reveal novel treatment targets. - 2024: Oxford: Raman micro-spectroscopy as a tool to study immunometabolism: Xu, J et al.
Conclusion: The synergy of Raman technologies with machine learning is poised to enhance the understanding of complex Raman phenotypes, enabling biomarker discovery and comprehensive investigations in immunometabolism. The review encourages further exploration of these evolving technologies in the rapidly advancing field of immunometabolism. - 2023: Liverpool: Home-based testing protocol to measure physiological responses to everyday activities in ME: a feasibility study: Clague-Baker, N et al.
Conclusion: Physiological measurement during everyday activities was feasible for our participants who represented a range of ME severities. Activities must be adapted for different levels of severity to avoid significant symptom exacerbation. Further research is needed to develop home-based assessment protocols to advance the biobehavioral understanding of ME. - 2023: London: Long COVID: mechanisms, risk factors and recovery: Astin, R et al.
Conclusion: Rehabilitation can be effective but presents a resource challenge in providing sufficient monitoring to match activity to physiological capabilities to avoid exacerbating damage. Pharmacological treatments are likely to only be effective in subpopulations of patients with specific symptoms and underlying pathology. Multi-disciplinary approaches spanning epidemiology, immunology, multi-system physiology and clinical research are therefore required to understand the different, interacting processes at play and to understand how to best combat them to restore health. - 2023: Oxford: Developing a Blood Cell-based Diagnostic Test for ME/CFS Using PBMCs: Huang, W et al.
Conclusion: Further investigations to evaluate model performance in extended cohorts of patients, to identify the precise ME/CFS EV components detected by Raman and to reveal their functional significance in the disease are warranted. - 2022: Valencia: Diagnosis of ME/CFS with Partial Least Squares Discriminant Analysis: Relevance of Blood Extracellular Vesicles: Gonzalez-Cebrian, A et al.
Conclusion: These results demonstrate that Raman profiles of blood cells can distinguish between healthy individuals, disease controls, and ME/CFS patients with high accuracy (91%), and can further differentiate between mild, moderate, and severe ME/CFS patients (84%). - 2021: Torun: Relationship between Cardiopulmonary, Mitochondrial and Autonomic Nervous System Function Improvement after an Individualised Activity Programme upon CFS patients: Kujawski, S et al.
Conclusion: It is concluded that the Individualised Activity Program (IAP) reduces fatigue and improves functional performance along with changes in autonomic and mitochondrial function. However, caution must be applied as exercise was not well tolerated by 51% of patients. - 2021: Valencia: Induced Pluripotent Stem Cells as Suitable Sensors for FM and ME/CFS: Monzón-Nomdedeu, MB et al.
Conclusion: This opinion review explains our hypothesis that induced pluripotent stem cells (iPSCs) could be developed as a screening platform to provide evidence of a metabolic imbalance in FM and ME/CFS. - 2020: Valencia: Assessing Diagnostic Value of MicroRNAs from PBMCs and EVs in ME/CFS: Almenar-Perez, E et al.
Conclusion: Our results show that routine creatine kinase (CK) blood values, plasma EVs physical characteristics (including counts, size and zeta-potential), and a limited number of differentially expressed PBMC and EV miRNAs appear significantly associated with severe ME/CFS (p < 0.05). - 2020: Toruń: Autonomic Phenotypes in CFS are Associated with Illness Severity: A Cluster Analysis: Słomko, J et al.
Conclusions: (a) identifying autonomic symptomatology in patients with CFS will contribute to the understanding of the role that the ANS plays in CFS pathophysiology (b) subjective and/or objective autonomic function measurement should be required during the diagnostic process (c) autonomic phenotypes in CFS patients are strongly associated with measures of illness severity, suggesting that different approaches to treatment might be warranted. - 2019: Brussels: Relationship Between Exercise-induced Oxidative Stress Changes and Parasympathetic Activity in CFS: An Observational Study in Patients and Healthy Subjects: Polli, A et al.
Conclusion: While we found no exercise-induced changes in oxidative stress, we found consistent associations between pain symptoms and oxidative stress in patients with ME/CFS. On the contrary, there was a strong association between exercise-induced changes in ANS and oxidative stress changes in healthy controls. The more that parasympathetic activity increases following exercise, the greater the reduction in oxidative stress. We suggest that vagal activity exerts regulatory actions on oxidative stress during exercise. Patients with ME/CFS and other chronic pain conditions might lack this control, and that might account for the lack of exercise-induced hypoalgesia that is often found in these patients. Exploring these mechanisms could potentially lead to helpful and innovative treatments for chronic pain. - 2019: Manchester: The ‘Cognitive Behavioural Model’ of CFS: Critique of a Flawed Model: Geraghty, K et al.
Conclusion: Our findings suggest the CBM is not fit for purpose, as it poorly reflects the accounts given by patients and it ignores the wealth of evidence showing biological, immune and neurological dysfunction in ME/CFS. Given that the CBM is cited as the basis for CBT and GET interventions, there is an urgent need for clinicians, therapists and health providers to review this treatment paradigm. Our findings help explain why so many patients reject psychotherapy. An alternative model should be formulated to better explain the biological factors that predispose, precipitate and perpetuate the illness. - 2019: Newcastle: Assessing Cellular Energy Dysfunction in CFS/ME Using a Commercially Available Laboratory Test: Newton, J et al.
Conclusion: The MES test does not have the reliability and reproducibility required of a diagnostic test and therefore should not currently be offered as a diagnostic test for CFS/ME. The differences observed by the Myhill group may be down to differences in sample processing time between cohorts. - 2019: Newcastle: Mitochondrial Complex Activity in Permeabilised Cells of CFS Patients using Two Cell Types: Tomas, C et al.
Conclusion: The finding of normal mitochondrial functioning of CFS myotubes supports the results of unpublished data from whole cells (Rutherford, 2016). The results showing no difference in mitochondrial activity in permeabilised PBMCs were unexpected given that mitochondrial function in PBMCs has previously been shown to be significantly lower in CFS (Tomas et al., 2017). Given the results here, the future of bioenergetic studies in CFS should concentrate on mechanisms upstream of the mitochondrial respiratory chain. - 2019: Oxford: Impact of pharmacological agents on mitochondrial function: a growing opportunity?: Stoker, M et al.
Conclusion: Mitochondrial dysfunction results from off-target effects from these drugs rather than being the main mode of action; however, we have shown that modulating mitochondrial function could be beneficial in the treatment of a variety of diseases such as cancer, diabetes and chronic viral infection. - 2019: Toruń: The Impact of a Structured Exercise Programme upon Cognitive Function in CFS Patients: Zalewski, P et al.
Conclusion: A substantial number of participants were unwilling or unable to complete the exercise programme. ME/CFS patients able to complete the structured exercise programme (SEP) showed improved visual attention both in terms of reaction time and correctness of responses and processing speed of simple visual stimuli. - 2018: Manchester: ME/CFS and the Biopsychosocial Model: A Review of Patient Harm and Distress in the Medical Encounter: Geraghty, K et al.
Conclusion: The biopsychosocial framework currently applied to ME/CFS is too narrow in focus and fails to adequately incorporate the patient narrative. Misdiagnosis, conflict, and harm are observable outcomes where doctors’ and patients’ perspectives remain incongruent. Biopsychosocial practices should be scrutinized for potential harms. Clinicians should consider adopting alternative patient-centred approaches. - 2018: Oxford: Potential clinical usefulness of gut microbiome testing in a variety of clinical conditions: Morten, K et al.
Conclusion: In this study we investigated microbiome diversity in a range of conditions including cancer, ME/CFS, IBS, and obesity among others. Potential clinical effectiveness of the diversity score applicable to a wide range of medical conditions, has greater sensitivity and reduces multiple testing compared to bacteria taxa comparisons. Faecal microbiome testing is clinically useful and potentially defines treatment directions in a particular patient. - 2018: Oxford: A New Approach to Find Biomarkers in CFS/ME by Single-cell Raman Micro-spectroscopy: Xu, J et al.
Conclusion: A machine learning classification model achieved an accuracy rate of 98% correctly assigning Raman spectra to either the CFS group or the control group. SCRM combined with a machine learning algorithm therefore has the potential to become a diagnostic tool for CFS. - 2017: Koper: The Role of Autonomic Function in Exercise-induced Endogenous Analgesia: A Case-control Study in ME/CFS: Oosterwijck, JV et al.
Conclusion: Reduced parasympathetic reactivation during recovery from exercise is associated with the dysfunctional exercise-induced analgesia in ME/CFS. Poor recovery of diastolic blood pressure in response to exercise, with blood pressure remaining elevated, is associated with reductions of pain following exercise in ME/CFS, suggesting a role for the arterial baroreceptors in explaining dysfunctional exercise-induced analgesia in ME/CFS patients. - 2017: Manchester: ME/CFS Patients’ Reports of Symptom Changes following CBT, GET and Pacing treatments: Analysis of a Primary Survey Compared with Secondary Surveys: Geraghty, K et al.
Conclusion: Findings from analysis of primary and secondary surveys suggest that CBT is of benefit to a small percentage of patients (8%-35%), GET brings about large negative responses in patients (54%-74%), while Pacing is the most favoured treatment with the lowest negative response rate and the highest reported benefit (44%-82%) . - 2017: Newcastle: Cellular Bioenergetics is Impaired in Patients with CFS: Tomas, C et al.
Conclusion: The metabolic differences discovered highlight the inability of CFS patient PBMCs to fulfil cellular energetic demands both under basal conditions and when mitochondria are stressed during periods of high metabolic demand. - 2017: Potchefstroom: Clinically proven mtDNA mutations are not common in those with CFS: Schoeman, EM et al.
Conclusion: The work supports the assertion that CFS should not be considered to fall within the spectrum of mtDNA disease. However, the current study cannot exclude a role for nuclear genes with a mitochondrial function, nor a role of mtDNA population variants in susceptibility to disease. This study highlights the need for more to be done to understand the pathophysiology of CFS. - 2016: Northumbria: The experience of sleep in CFS: A qualitative interview study with patients: Gotts, Z et al.
Conclusion: Each patient with CFS has a unique experience of sleep. Despite the differing narratives regarding the role of sleep in CFS, all participants held the belief that sleep is a vital process for health and well-being which has had a direct bearing on the course and progression of their CFS. Also, every participant regarded their sleep as in some way ‘broken’ and in need of management/repair. Patients’ insights demonstrate sleep-specific influences on their CFS, and the impact of disturbed sleep should be a consideration for clinical and research work. - 2011: Newcastle: Loss of Capacity to Recover from Acidosis on Repeat Exercise in CFS: A Case-control Study: Jones, DEJ et al.
Conclusion: When exercising to comparable levels to normal controls, CFS patients exhibit profound abnormality in bioenergetic function and response to it. Although exercise intervention is the logical treatment for patients showing acidosis, any trial must exclude subjects who do not initiate exercise as they will not benefit. This potentially explains previous mixed results in CFS exercise trials. - 2009: Buckinghamshire: Risk Factors for Severe ME/CFS: Pheby, D et al.
Conclusion: Exposure to potential risk factors, including familial risks, personality, and early management of the illness, was compared in 124 people with severe disease and 619 mildly ill controls. Early management of the illness appeared the most important determinant of severity. Having a mother with ME/CFS was also important. Smoking and personality were not risk factors, neurotic traits being more frequent among the less severely ill. Conscientiousness overall was not related to severity. - 2009: Glasgow: A Gene Signature for Post-Infectious CFS: Gow, J et al.
Conclusion: Differential expression of key genes identified in this study offer an insight into the possible mechanism of chronic fatigue following infection. The representative biomarkers identified in this research appear promising as potential biomarkers for diagnosis and treatment. - 2008: London: Dietary Intervention in Chronic Fatigue Syndrome: Hobday, RA et al.
Conclusion: In this randomized control trial, a Low Sugar Low Yeast (LSLY) diet appeared to be no more efficacious on levels of fatigue or QoL compared to Healthy Eating (HE). Given the difficulty with dietary compliance experienced by participants, especially in the LSLY group, it would appear HE guidance is a more pragmatic approach than advocating a complicated dietary regime. - 2007: Liverpool: The Role of Cytokines in Muscle Fatigue in Patients with CFS: McArdle, A et al.
Conclusion: This preliminary data suggests that a sub-group of patients with CFS may have low level inflammation and analyses are underway to further characterise other inflammatory markers in serum and muscle of these patients and to determine whether such changes could affect indices of muscle function or central fatigue. - 2006: CFSUM1 and CFSUM2 in Urine from Patients with CFS are Methodological Artefacts: Chalmers, RA et al.
Conclusion: Both CFSUM1 and CFSUM2 are artefacts of the sample preparation procedure and previously reported quantitative abnormalities of CFSUM1 and CFSUM2 in urine from patients with ME/CFS are also artefactual. Pyroglutamic acid may be of primarily dietary origin. The methods used cannot provide reliable qualitative or quantitative data on urinary metabolites. No clinical or biochemical significance can be drawn between these compounds in ME/CFS or any other clinical conditions. - 2005: London: Plasma and Urinary Carnitine and Acylcarnitines in Chronic Fatigue Syndrome: Jones, MG et al.
Conclusion: The data presented here show that, in the CFS patients studied, there are no significant abnormalities of free or esterified (acyl) carnitine. It is thus unlikely that abnormalities in carnitine homeostasis have any significant role in the aetiology of their chronic fatigue. - 2005: London: Urinary and plasma organic acids and amino acids in chronic fatigue syndrome: Jones, MG et al.
Conclusion: None of the previously reported abnormalities in urinary amino acids or of organic acids could be confirmed. Results however provide some evidence in patients with ME/CFS for underlying inflammatory disease and for reduced intramuscular collagen with a lowered threshold for muscle micro-injury. These factors in combination may provide a basis for the fatigue and muscle pain that are the major symptoms in these patients. - 2003: Dundee: Prolonged acetylcholine-induced vasodilatation in the peripheral microcirculation of patients with CFS: Khan, F et al.
Conclusion: No differences in peak blood flow was seen between patients and controls, but the time taken for the ACh response to recover to baseline was significantly longer in the CFS patients than in control subjects. Prolongation of ACh-induced vasodilatation is suggestive of a disturbance to cholinergic pathways, perhaps within the vascular endothelium of patients with CFS, and might be related to some of the unusual vascular symptoms, such as hypotension and orthostatic intolerance, which are characteristic of the condition. - 2003: Glasgow: Proton magnetic resonance spectroscopy of basal ganglia in Chronic Fatigue Syndrome: Chaudhuri, A et al.
Conclusion: Fatigue is a common symptom of neurological diseases that affect basal ganglia function. A highly significant increase in the spectra from choline-containing compounds was seen in the CFS patient group (p < 0.001). In the absence of regional structural or inflammatory pathology, increased choline resonance in CFS may be an indicator of higher cell membrane turnover due to gliosis or altered intramembrane signalling. - 2003: Glasgow: Chronic Fatigue Syndrome: New Evidence for a Central Fatigue Disorder: Georgiades, E et al.
Conclusion: The significant differences observed in a number of key putative CNS 5-HT and dopaminergic modulators, coupled with the exacerbated perception of effort, provide further evidence for a potentially significant role for CNS mechanisms in the pathogenesis of CFS. - 2001: Glasgow: Antiviral Pathway Activation in Patients with CFS and Acute Infection: Gow, J et al.
Conclusion: Pathway activation in the group of patients with infections differed significantly from that of the other 2 groups, in whom there was no evidence of upregulation. Therefore, assay of activation is unlikely to provide the basis for a diagnostic test for CFS.