Cellular Chain Reaction May Drive Low Energy in ME/CFS Patients
Researchers identified an immune cell defect that may drive ME/CFS symptoms.
In a world first, Griffith University researchers have identified a key immune cell dysfunction in people with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), offering new clues on the condition.
The study addressed a critical question: Are the mitochondrial deficits reported by other researchers a downstream consequence of the ion‑channel and calcium abnormalities previously identified?
Lead author, PhD Candidate Chandi Magawa, and the research team from Griffith’s National Centre for Neuroimmunology and Emerging Diseases (NCNED), used advanced live‑cell imaging to observe TRPM3‑dependent calcium movement into mitochondria in real time.
“We found a significant TRPM3-calcium pathway dysfunction in ME/CFS, resulting in impaired calcium entry into mitochondria, a region of the cell responsible for energy production,” she said.
“It explains how reduced calcium entry into mitochondria may impair immune cell function and energy production, the process effectively triggering a chain reaction in the body.”
Dr Natalie Eaton-Fitch said ME/CFS was a serious and complex condition in which there was no cure or treatment.
“The latest data from the Australian Institute of Health and Welfare estimates 219,000 Australians are living with the illness,” she said.
Symptoms included profound, persistent exhaustion; post-exertional malaise, pain, cognitive difficulties, dizziness, temperature instability and sensory sensitivity, which could severely restrict day-to-day functioning, education, employment and social participation.
NCNED Director, Professor Sonya Marshall-Gradisnik, said the study helped to explain the underlying biological dysfunction, moving the condition further away from being misunderstood or dismissed.
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