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Protein Modification: A Proposed Mechanism for the Long-Term Pathogenesis of Traumatic Brain Injury

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Technical Report

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Uniformed Services University Of The Health Sciences Bethesda United States

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Traumatic brain injury TBI is a major cause of long-term disability. Acute TBI prompts a constellation of dysfunctional processes, collectively known as secondary injury mechanisms. A hallmark secondary injury in TBI is a prolonged imbalance in calcium homeostasis, resulting in a dramatic influx of calcium into brain cells. This influx elicits the generation of damaging reactive oxygen species. Protein carbonylation and citrullination are pathological post-translational modifications that can result from intracellular calcium overload. These modifications have been proposed to play a role in neurodegenerative disorders, including Alzheimers disease, and multiple sclerosis. Both carbonylation and citrullination can contribute to ongoing dysfunction, either through direct loss of protein function or via immune-based mechanisms where proteins specifically modified by citrullination become targeted by the adaptive immune system. This work investigated carbonylation and citrullination in a rodent model of TBI. We have identified specific regions and cell types susceptible to these modifications following TBI.

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