Hypoaminoacidemia Characterizes Chronic Traumatic Brain Injury

William J. Durham, Jack P. Foreman, Kathleen M. Randolph, Christopher P. Danesi, Heidi Spratt, Brian Masel, Jennifer R. Summons, Charan K. Singh, Melissa Morrison, Claudia Robles, Cindy Wolfram, Lisa A. Kreber, Randall Urban, Melinda Sheffield-Moore, Brent E. Masel

Research output: Contribution to journalArticle

Abstract

Individuals with a history of traumatic brain injury (TBI) are at increased risk for a number of disorders, including Alzheimer's disease, Parkinson's disease, and chronic traumatic encephalopathy. However, mediators of the long-term morbidity are uncertain. We conducted a multi-site, prospective trial in chronic TBI patients (∼18 years post-TBI) living in long-term 24-h care environments and local controls without a history of head injury. Inability to give informed consent was exclusionary for participation. A total of 41 individuals (17 moderate-severe TBI, 24 controls) were studied before and after consumption of a standardized breakfast to determine if concentrations of amino acids, cytokines, C-reactive protein, and insulin are potential mediators of long-term TBI morbidity. Analyte concentrations were measured in serum drawn before (fasting) and 1 h after meal consumption. Mean ages were 44 ± 15 and 49 ± 11 years for controls and chronic TBI patients, respectively. Chronic TBI patients had significantly lower circulating concentrations of numerous individual amino acids, as well as essential amino acids (p = 0.03) and large neutral amino acids (p = 0.003) considered as groups, and displayed fundamentally altered cytokine-amino acid relationships. Many years after injury, TBI patients exhibit abnormal metabolic responses and altered relationships between circulating amino acids, cytokines, and hormones. This pattern is consistent with TBI, inducing a chronic disease state in patients. Understanding the mechanisms causing the chronic disease state could lead to new treatments for its prevention.

Original languageEnglish (US)
Pages (from-to)385-390
Number of pages6
JournalJournal of Neurotrauma
Volume34
Issue number2
DOIs
StatePublished - Jan 15 2017

Fingerprint

Chronic Brain Injury
Amino Acids
Cytokines
Chronic Disease
Morbidity
Neutral Amino Acids
Traumatic Brain Injury
Essential Amino Acids
Breakfast
Informed Consent
Craniocerebral Trauma
C-Reactive Protein
Parkinson Disease
Meals
Fasting
Alzheimer Disease

Keywords

  • head trauma
  • metabolism

ASJC Scopus subject areas

  • Clinical Neurology

Cite this

Durham, W. J., Foreman, J. P., Randolph, K. M., Danesi, C. P., Spratt, H., Masel, B., ... Masel, B. E. (2017). Hypoaminoacidemia Characterizes Chronic Traumatic Brain Injury. Journal of Neurotrauma, 34(2), 385-390. https://doi.org/10.1089/neu.2015.4350

Hypoaminoacidemia Characterizes Chronic Traumatic Brain Injury. / Durham, William J.; Foreman, Jack P.; Randolph, Kathleen M.; Danesi, Christopher P.; Spratt, Heidi; Masel, Brian; Summons, Jennifer R.; Singh, Charan K.; Morrison, Melissa; Robles, Claudia; Wolfram, Cindy; Kreber, Lisa A.; Urban, Randall; Sheffield-Moore, Melinda; Masel, Brent E.

In: Journal of Neurotrauma, Vol. 34, No. 2, 15.01.2017, p. 385-390.

Research output: Contribution to journalArticle

Durham, WJ, Foreman, JP, Randolph, KM, Danesi, CP, Spratt, H, Masel, B, Summons, JR, Singh, CK, Morrison, M, Robles, C, Wolfram, C, Kreber, LA, Urban, R, Sheffield-Moore, M & Masel, BE 2017, 'Hypoaminoacidemia Characterizes Chronic Traumatic Brain Injury', Journal of Neurotrauma, vol. 34, no. 2, pp. 385-390. https://doi.org/10.1089/neu.2015.4350
Durham, William J. ; Foreman, Jack P. ; Randolph, Kathleen M. ; Danesi, Christopher P. ; Spratt, Heidi ; Masel, Brian ; Summons, Jennifer R. ; Singh, Charan K. ; Morrison, Melissa ; Robles, Claudia ; Wolfram, Cindy ; Kreber, Lisa A. ; Urban, Randall ; Sheffield-Moore, Melinda ; Masel, Brent E. / Hypoaminoacidemia Characterizes Chronic Traumatic Brain Injury. In: Journal of Neurotrauma. 2017 ; Vol. 34, No. 2. pp. 385-390.
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