Journal
BIOMEDICINES
Volume 10, Issue 7, Pages -Publisher
MDPI
DOI: 10.3390/biomedicines10071718
Keywords
chronic traumatic encephalopathy (CTE); non-targeted metabolomics; astrocyte activation; catecholamines; tyrosine metabolism; phenylalanine metabolism
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Funding
- Intramural Research Program of the Korea Institute of Science and Technology (KIST) [2E31623, 2E31504, 2E31505]
- Korean National Research Foundation [NRF-2018M3C7A1056894, NRF-2020M3E5D9079742, NRF-2022R1A2C3013138, 2022R1A2C3003901]
- NIH [R01NS109537]
- National Research Foundation of Korea [2022R1A2C3003901, 2018M3C7A1056894] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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This study utilized metabolomics to uncover the metabolic differences associated with cognitive dysfunction, amyloid-beta deposition, and neuroinflammation in the brains of patients with chronic traumatic encephalopathy (CTE). These findings provide new insights into the pathogenesis of CTE and suggest potential targets for diagnosis and treatment.
Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease that is frequently found in athletes and those who have experienced repetitive head traumas. CTE is associated with a variety of neuropathologies, which cause cognitive and behavioral impairments in CTE patients. However, currently, CTE can only be diagnosed after death via brain autopsy, and it is challenging to distinguish it from other neurodegenerative diseases with similar clinical features. To better understand this multifaceted disease and identify metabolic differences in the postmortem brain tissues of CTE patients and control subjects, we performed ultra-high performance liquid chromatography-mass spectrometry (UPLC-MS)-based non-targeted metabolomics. Through multivariate and pathway analysis, we found that the brains of CTE patients had significant changes in the metabolites involved in astrocyte activation, phenylalanine, and tyrosine metabolism. The unique metabolic characteristics of CTE identified in this study were associated with cognitive dysfunction, amyloid-beta deposition, and neuroinflammation. Altogether, this study provided new insights into the pathogenesis of CTE and suggested appealing targets for both diagnosis and treatment for the disease.
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