Here we report preliminary data demonstrating that some patients with
myalgic encephalomyelitis/chronic fatiguesyndrome (ME/CFS) may have catalytic
autoantibodies that cause the breakdown of
myelin basic protein (MBP). We propose that these MBP-degradative
antibodies are important to the pathophysiology of ME/CFS, particularly in the occurrence of
white matter disease/
demyelination. This is supported by magnetic resonance imagining studies that show these findings in patients with ME/CFS and could explain symptoms of
nerve pain and
muscle weakness. In this work, we performed a series of experiments on patient plasma samples where we isolated and characterized substrate-specific
antibodies that digest MBP. We also tested
glatiramer acetate (
copaxone), an FDA approved
immunomodulator to treat
multiple sclerosis, and found that it inhibits ME/CFS antibody digestion of MBP. Furthermore, we found that
aprotinin, which is a specific
serine protease inhibitor, specifically prevents breakdown of MBP while the other classes of
protease inhibitors had no effect. This coincides with the published literature describing
catalytic antibodies as having
serine protease-like activity. Postpandemic research has also provided several reports of
demyelination in
COVID-19. Because
COVID-19 has been described as a trigger for ME/CFS,
demyelination could play a bigger role in patient symptoms for those recently diagnosed with ME/CFS. Therefore, by studying proteolytic
antibodies in ME/CFS, their target substrates, and inhibitors, a new mechanism of action could lead to better treatment and a possible cure for the disease.