Griffith researchers move one step closer to understanding cause of Chronic Fatigue Syndrome

A new finding in the cause of Chronic Fatigue Syndrome (CFS) has been identified by researchers at Griffith University who say they are getting much closer to a complete understanding of this disabling condition.

This is the news from a team at the National Centre for Neuroimmunology and Emerging Diseases at the Menzies Health Institute Queensland, where a research team has identified significant impairments in the cellular function of people with CFS.

CFS – sometimes known as ME (myalgic encephalomyelitis) – is a complex illness characterised by impaired memory and concentration, metabolic, cardiac, gut and immune dysfunction and debilitating muscle pain and fatigue on exertion (also known as neuroimmune exhaustion).

Published in Biological Research, (https://biolres.biomedcentral.com/articles/10.1186/s40659-016-0087-2) the study reveals a receptor not previously identified on particular immune cells.

"TRPM3 receptors have been identified on these particular immune cells, not only in healthy people for the first time, but also have been shown to be significantly reduced in CFS/ME patients," says Professor Sonya Marshall-Gradisnik who is leading the study.

"These receptors are important as they move calcium inside the cell. Interestingly in this study we also reported a significant reduction of calcium inside these cells from CFS/ME patients.

"The discovery means that we now have a potentially key contributing factor in the cause of this condition. This discovery also fits with our previous research showing that changes in genes and cell function are involved in vital cell signalling pathways found in all cell types."

"These findings contribute to our knowledge of the clinical presentation of this condition and provide a sound basis for further research," says Professor Don Staines. "We are now much closer to having a complete understanding of CFS."

In another recent publication Clinical Therapeutics, NCNED researchers have shown that few therapeutic interventions are currently effective in CFS/ME.

"This is a very complex illness and it is likely that no single intervention will counter all effects of the pathology. We need to have concentrated efforts on further research to discover appropriate treatments which are effective," Professor Staines says.

In the coming weeks these novel research findings are being presented by NCNED researchers at international clinical and research conferences in London and the Federation of America Societies For Experiential Biology (FASEB), Lisbon.

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