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Metabolites 2018, 8(3), 50; https://doi.org/10.3390/metabo8030050

Potential Metabolomic Linkage in Blood between Parkinson’s Disease and Traumatic Brain Injury

1
Translational Laboratory and Biorepository, Department of Neurology, University of California Irvine School of Medicine, Irvine, CA 92697-3910, USA
2
Department of Neurological Surgery, University of California Irvine School of Medicine, Irvine, CA 92697-3910, USA
3
Department of Anatomy & Neurobiology, University of California Irvine School of Medicine, Irvine, CA 92697-3910, USA
4
Intrepid Spirit Concussion Recovery Center, Naval Medical Center Camp Lejeune, Jacksonville, NC 28540, USA
5
Nuffield Department of Clinical Neurosciences, University of Oxford, 01865 Oxford, UK
6
Department of Neurology, John Radcliffe Hospital, Oxford University Hospitals Trust, Oxford 01865, UK
7
Department of Physiology, Anatomy and Genetics, Oxford Parkinson’s Disease Centre, University of Oxford, Oxford 01865, UK
8
Department of Emergency Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY 14604, USA
9
Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC 20001, USA
10
Department of Biochemistry and Molecular & Cellular Biology, Georgetown University Medical Center, Washington, DC 20001, USA
*
Authors to whom correspondence should be addressed.
Received: 24 July 2018 / Revised: 1 September 2018 / Accepted: 4 September 2018 / Published: 7 September 2018
(This article belongs to the Special Issue Metabolomics in Neurodegenerative Disease)
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Abstract

The etiologic basis for sporadic forms of neurodegenerative diseases has been elusive but likely represents the product of genetic predisposition and various environmental factors. Specific gene-environment interactions have become more salient owing, in part, to the elucidation of epigenetic mechanisms and their impact on health and disease. The linkage between traumatic brain injury (TBI) and Parkinson’s disease (PD) is one such association that currently lacks a mechanistic basis. Herein, we present preliminary blood-based metabolomic evidence in support of potential association between TBI and PD. Using untargeted and targeted high-performance liquid chromatography-mass spectrometry we identified metabolomic biomarker profiles in a cohort of symptomatic mild TBI (mTBI) subjects (n = 75) 3–12 months following injury (subacute) and TBI controls (n = 20), and a PD cohort with known PD (n = 20) or PD dementia (PDD) (n = 20) and PD controls (n = 20). Surprisingly, blood glutamic acid levels in both the subacute mTBI (increased) and PD/PDD (decreased) groups were notably altered from control levels. The observed changes in blood glutamic acid levels in mTBI and PD/PDD are discussed in relation to other metabolite profiling studies. Should our preliminary results be replicated in comparable metabolomic investigations of TBI and PD cohorts, they may contribute to an “excitotoxic” linkage between TBI and PD/PDD. View Full-Text
Keywords: Parkinson’s disease; Parkinson’s disease dementia; subacute mild traumatic brain injury; glutamic acid; excitotoxicity; metabolomics Parkinson’s disease; Parkinson’s disease dementia; subacute mild traumatic brain injury; glutamic acid; excitotoxicity; metabolomics
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Fiandaca, M.S.; Gross, T.J.; Johnson, T.M.; Hu, M.T.; Evetts, S.; Wade-Martins, R.; Merchant-Borna, K.; Bazarian, J.; Cheema, A.K.; Mapstone, M.; Federoff, H.J. Potential Metabolomic Linkage in Blood between Parkinson’s Disease and Traumatic Brain Injury. Metabolites 2018, 8, 50.

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