Myocyte ME/CFS Plasma Exposure

Fatigue is a non-specific symptom of many diseases and conditions such as stroke, Parkinson’s, cancers, psychiatric disorders (bipolar), multiple sclerosis, rheumatoid arthritis, heart failure and hepatitis C. Patients undergone chemotherapy has also reported fatigue as part of the side-effects of the treatment. Current research published show that patients with ME/CFS have deficiencies with energy metabolism and mitochondrial dysfunction. Glucose transport? There have been reports of an immunological aspect of fatigue.

Within the Morten Group the research is primarily focused on unravelling the mechanisms behind mitochondrial dysfunction and the impedance of energy metabolism. We have access to samples obtained from patients with a range of ME/CFS functional capacities and also samples from healthy controls. Currently we have funding in place to use these samples to investigate the mitochondrial contribution in the role of fatigue. The lack of research into the understanding the molecular causes of fatigue in any disease or as a side-effect of drug therapy is vastly underfunded. Thus our understanding of fatigue mechanism is lacking and is a limiting factor for the development of treatments and biomarkers for conditions such as ME/CFS.

The mitochondria’s function goes far beyond the classical role of ATP production and energy metabolism. The organelle plays central roles in cell survival, signal transductions and redox homeostasis. The mitochondrion fuses together and forms a mitochondrial network. This network is dynamic, responding to overall cellular needs and tightly controlled by several key proteins. In recent years it has become evident that the regulation of mitochondrial biogenesis and network dynamics is of great importance to cellular physiology in health and disease.  

To better understand the effect disease and drug treatments have on the mitochondrial network morphology, the Morten Group use the InCell Analyzer (GE Healthcare) to investigate the changes in the network in for example primary fibroblasts from patients and healthy controls.

The mitochondria houses key pathways for the production of ATP and these pathways can be affected by changes to the network. In addition to the InCell method we have assays that examine changes to the electron transport chain.

We have access to a range of different cell types, from primary human tissue and immortalized cell lines.