Myalgic encephalomyelitis, long trivialised under the label chronic fatigue syndrome, is a multi-system disease with no effective treatment and a hallmark feature: post-exertional malaise, in which minor physical, mental or emotional effort can worsen symptoms for hours, days or weeks. About 75 per cent of cases follow a viral infection, from Epstein-Barr to SARS-CoV-2. Alain Moreau, professor of biochemistry and molecular medicine at Université de Montréal and researcher at CHU Sainte-Justine, leads one of the field's most ambitious research programmes.
Moreau's molecular analyses suggest that up to 40 per cent of people diagnosed with ME may actually have fibromyalgia, and the two conditions can coexist, a finding with immediate consequences for diagnosis. His team has identified SMPDL3B, a circulating protein whose levels track symptom severity, reported in the Journal of Translational Medicine, together with microRNA signatures that can distinguish ME from fibromyalgia. A further study argues that epigenetic changes triggered by infections and toxins offer a more promising explanation than genetic variants alone.
Having pinpointed the enzyme responsible for raising SMPDL3B levels, the team is exploring whether existing diabetes drugs combined with myo-inositol could inhibit it, with clinical trials in planning. The rise of long COVID, which closely resembles other post-infectious syndromes, has pushed ME up the research agenda. For a patient community long told the illness was in their heads, measurable biology, including evidence of neuroinflammation, is proving quietly transformative.