Thursday, March 16, 2017

New CDMRP Study Finds More Evidence of Neuroinflammation, injury in Gulf War Illness

( - Mar. 16, 2017) - A new study released this week ahead of publication shows further evidence of neuroinflammation and injury to the cells of the brain, neurons, following Gulf War toxic exposures.  The study also confirmed the continuing presence of gliosis, nonspecific evidence of injury to the brain or spinal cord and commonly found in other neurological diseases.

The study was led by Dr. Kimberly Sullivan of Boston University and. Dr. Mohammed Abou-Donia of Duke University.

It was funded by the treatment-focused Gulf War Illness Research Program (GWIRP), part of the Congressionally Directed Medical Research Program (CDMRP) funded by Congress under the U.S. Department of Defense health program.

It also incorporated data from a GWIRP-funded treatment study by Dr. Lisa Conboy of acupuncture, which showed good success in helping to reduce pain related to Gulf War Illness.

Sullivan also leads the Gulf War Illness Consortium (GWIC) at Boston University, a very large GWIRP-funded project that is currently recruiting up to 300 healthy and ill veterans of the 1991 Gulf War (Operation Desert Storm) in Boston, Houston, and Miami.   Participation in the study will help as many as 250,000 fellow Gulf War veterans who remain ill, and may also help other veterans who have suffered similar toxic exposures.

Abou-Donia performed some of the earliest Gulf War Illness research, funded by Ross Perot, that showed that damage in laboratory animals by Gulf War chemical agents mirrored Gulf War Illness health effects.

Validation efforts of the biomarkers identified in the study are already in progress.  

-Anthony Hardie,


SOURCE:  PubMed, ePub ahead of publication, Mar. 9, 2017


 2017 Mar 9. pii: S0892-0362(17)30050-8. doi: 10.1016/ [Epub ahead of print]

Screening for novel central nervous system biomarkers in veterans with Gulf War Illness.


Gulf War illness (GWI) is primarily diagnosed by symptom report; objective biomarkers are needed that distinguish those with GWI. Prior chemical exposures during deployment have been associated in epidemiologic studies with altered central nervous system functioning in veterans with GWI. Previous studies from our group have demonstrated the presence of autoantibodies to essential neuronal and glial proteins in patients with brain injury and autoantibodies have been identified as candidate objective markers that may distinguish GWI. Here, we screened the serum of 20 veterans with GWI and 10 non-veteran symptomatic (low back pain) controls for the presence of such autoantibodies using Western blot analysis against the following proteins: neurofilament triplet proteins (NFP), tubulin, microtubule associated tau proteins (Tau), microtubule associated protein-2 (MAP-2), myelin basic protein (MBP), myelin associated glycoprotein (MAG), glial fibrillary acidic protein (GFAP), calcium-calmodulin kinase II (CaMKII) and glial S-100B protein. Serum reactivity was measured as arbitrary chemiluminescence units. As a group, veterans with GWI had statistically significantly higher levels of autoantibody reactivity in all proteins examined except S-100B. Fold increase of the cases relative to controls in descending order were: CaMKII 9.27, GFAP 6.60, Tau 4.83, Tubulin 4.41, MAG 3.60, MBP 2.50, NFP 2.45, MAP-2 2.30, S-100B 1.03. These results confirm the continuing presence of neuronal injury/gliosis in these veterans and are in agreement with the recent reports indicating that 25years after the war, the health of veterans with GWI is not improving and may be getting worse. Such serum autoantibodies may prove useful as biomarkers of GWI, upon validation of the findings using larger cohorts.


Autoantibodies; Brain injury; Cytoskeletal proteins; Gulf War Illness; Serum biomarkers

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