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J Neurotrauma. 2016 Jul 1;33(13):1270-7. doi: 10.1089/neu.2015.3881. Epub 2016 Feb 1.

Plasma Anti-Glial Fibrillary Acidic Protein Autoantibody Levels during the Acute and Chronic Phases of Traumatic Brain Injury: A Transforming Research and Clinical Knowledge in Traumatic Brain Injury Pilot Study.

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1 Departments of Psychiatry and Neuroscience, University of Florida , Gainesville, Florida.
2 Brain and Spinal Injury Center, San Francisco General Hospital , San Francisco, California.
3 Department of Neurological Surgery, University of California , San Francisco, San Francisco, California.
4 Department of Neurological Surgery, University of Pittsburgh Medical Center , Pittsburgh, Pennsylvania.
5 Department of Neurology, Uniformed Services University of the Health Sciences , and Center for Neuroscience and Regenerative Medicine, Bethesda, Maryland.
6 Department of Public Health, Erasmus Medical Center , Rotterdam, The Netherlands .
7 Department of Radiology, University of California , San Francisco, San Francisco, California.
8 Seton Brain and Spine Institute , Austin, Texas.
9 Department of Rehabilitation Medicine, Mount Sinai School of Medicine , New York, New York.
10 Department of Neurosurgery, Antwerp University Hospital , Edegem, Belgium .
11 Division of Anaesthesia, University of Cambridge and Addenbrooke's Hospital , Cambridge, United Kingdom .
12 Department of Psychology, University of Texas , Austin, Texas.


We described recently a subacute serum autoantibody response toward glial fibrillary acidic protein (GFAP) and its breakdown products 5-10 days after severe traumatic brain injury (TBI). Here, we expanded our anti-GFAP autoantibody (AutoAb[GFAP]) investigation to the multicenter observational study Transforming Research and Clinical Knowledge in TBI Pilot (TRACK-TBI Pilot) to cover the full spectrum of TBI (Glasgow Coma Scale 3-15) by using acute (<24 h) plasma samples from 196 patients with acute TBI admitted to three Level I trauma centers, and a second cohort of 21 participants with chronic TBI admitted to inpatient TBI rehabilitation. We find that acute patients self-reporting previous TBI with loss of consciousness (LOC) (n = 43) had higher day 1 AutoAb[GFAP] (mean ± standard error: 9.11 ± 1.42; n = 43) than healthy controls (2.90 ± 0.92; n = 16; p = 0.032) and acute patients reporting no previous TBI (2.97 ± 0.37; n = 106; p < 0.001), but not acute patients reporting previous TBI without LOC (8.01 ± 1.80; n = 47; p = 0.906). These data suggest that while exposure to TBI may trigger the AutoAb[GFAP] response, circulating antibodies are elevated specifically in acute TBI patients with a history of TBI. AutoAb[GFAP] levels for participants with chronic TBI (average post-TBI time 176 days or 6.21 months) were also significantly higher (15.08 ± 2.82; n = 21) than healthy controls (p < 0.001). These data suggest a persistent upregulation of the autoimmune response to specific brain antigen(s) in the subacute to chronic phase after TBI, as well as after repeated TBI insults. Hence, AutoAb[GFAP] may be a sensitive assay to study the dynamic interactions between post-injury brain and patient-specific autoimmune responses across acute and chronic settings after TBI.


autoantibody; autoimmunity; biomarkers; glia; traumatic brain injury

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