A new multi-institution study in the journal Neurotoxicology & Teretology, co-authored by a Boston University School of Public Health researcher, provides evidence that Gulf War Illness (GWI) stems from neuronal and glial injury affecting both the gray and white matter cells of the brain, and identifies serum autoantibodies that may prove useful as biomarkers of the illness.
The research team found “significantly elevated levels” of eight autoantibodies linked to certain central-nervous system cytoskeletal proteins (including tau, tubulin, myelin basic protein and glial fibrillary acidic protein) in a sample group of 20 Gulf War veterans, compared to a control group—a finding that suggests a “possible new avenue” for identifying an objective biomarker of Gulf War Illness. Glial fibrillary acidic protein—a marker of glial astrocyte injury—completely distinguished between the GWI cases and the controls in the study.
“These results confirm the presence of neuronal injury/glial activation in these veterans, and are in agreement with the recent reports indicating that 25 years after the war, the health of veterans with GWI is not improving and may be getting worse,” the authors said.
Study co-principal investigator Dr. Kimberly Sullivan, a research assistant professor of environmental health at BU and principal investigator on the Gulf War Illness Consortium project, which includes nine study sites, said the new study provides “objective, blood-based evidence of damage to the brains of sick Gulf War veterans. It indicates that, at least at some point, these veterans had a leaky blood-brain barrier that allowed these CNS proteins to enter their bloodstream and activate the immune system.”
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