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Further clues in the fight against chronic fatigue syndrome

Further clues in the fight against chronic fatigue syndrome

Further clues in the fight against chronic fatigue syndrome

Further clues in the fight against chronic fatigue syndrome

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New findings on the pathology of chronic fatigue syndrome (CFS) bring researchers closer to identifying the cause of this disabling illness -

This is the news from a team at the National Centre for Neuroimmunology and Emerging Diseases (NCNED)at the Menzies Health Institute Queensland.

See Also: Study finds brain abnormalities in chronic fatigue patients

Professors Marshall-Gradisnik and Don Staines and their research team have identified significant impairments in cellular function of people with CFS.

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

It is estimated that the prevalence rate of CFS/ME worldwide is between 1 and 2 percent.

"While the patho-mechanism of CFS/ME is unknown, these recent findings by NCNED researchers provide further evidence for the pathology of this illness," says Professor Sonya Marshall-Gradisnik, who speaks as we approach International CFS Awareness Day on Thursday May 12.

Published in the Journal of Translational Medicine, the results report significant differences in intracellular signalling of cells with CFS patients.

Learn More: Toward a clearer diagnosis of chronic fatigue syndrome

"In this group, we see that dysfunctional signalling may contribute to impaired cell activity. These findings are consistent with our previous findings and align with the presentation of symptoms in patients," says Professor Staines.

The current research findings build upon recent discoveries including novel identification of key genetic changes in cells of the immune system.

Note: Material may have been edited for length and content. For further information, please contact the cited source.

Griffith University


Huth TK, Staines D, Marshall-Gradisnik S. ERK1/2, MEK1/2 and p38 downstream signalling molecules impaired in CD56dimCD16+ and CD56brightCD16dim/− natural killer cells in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis patients.   Journal of Translational Medicine, Published April 21 2016. doi: 10.1186/s12967-016-0859-z