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Biomedicines
Special Issues
Advances Research in Traumatic Encephalopathy
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Advances Research in Traumatic Encephalopathy

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 20885

Special Issue Editor

Dr. Brandon Lucke-Wold

E-Mail Website
Guest Editor
Department of Neurosurgery, School of Medicine, West Virginia University, Morgantown, WV 26506, USA
Interests: traumatic brain injury; chronic traumatic encephalopathy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

The focus of this edition is on the advancements in understanding the pathology of traumatic encephalopathy and how these advances can be used to improve treatment. We are seeking articles related to fundamental “bench” research in addition to pharmaceutical advancement. In particular, we wish to focus on the pathological mechanisms of and treatment strategies for traumatic encephalopathy. Along these lines, we are also interested in articles discussing novel aspects of the pathophysiology related to the disease and how these molecular pathways may be targeted. Interdisciplinary team approaches attacking the problem from multiple different angles will be of interest to our readership. We are hoping to serve as a catalyst for sparking further discovery.

Dr. Brandon Lucke-Wold
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • traumatic brain injury
  • traumatic encephalopathy
  • mild traumatic brain injury
  • severe traumatic brain injury, closed or penetrating head injury
  • treatment advances

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Published Papers (5 papers)

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Editorial

Jump to: Research, Review

5 pages, 620 KiB  
Editorial
Advances Research in Traumatic Encephalopathy
by Sai Sriram and Brandon Lucke-Wold
Biomedicines 2022, 10(9), 2287; https://doi.org/10.3390/biomedicines10092287 - 15 Sep 2022
Cited by 4 | Viewed by 1514
Abstract
Though there are an abundance of chronic traumatic encephalopathy (CTE) cases worldwide [...] Full article
(This article belongs to the Special Issue Advances Research in Traumatic Encephalopathy)
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Research

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17 pages, 2492 KiB  
Article
Non-Targeted Metabolomics Approach Revealed Significant Changes in Metabolic Pathways in Patients with Chronic Traumatic Encephalopathy
by Jinkyung Lee, Suhyun Kim, Yoon Hwan Kim, Uiyeol Park, Junghee Lee, Ann C. McKee, Kyoung Heon Kim, Hoon Ryu and Jeongae Lee
Biomedicines 2022, 10(7), 1718; https://doi.org/10.3390/biomedicines10071718 - 15 Jul 2022
Cited by 2 | Viewed by 2552
Abstract
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 [...] Read more.
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. Full article
(This article belongs to the Special Issue Advances Research in Traumatic Encephalopathy)
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27 pages, 5688 KiB  
Article
Characterisation of Severe Traumatic Brain Injury Severity from Fresh Cerebral Biopsy of Living Patients: An Immunohistochemical Study
by Ping K. Yip, Shumaila Hasan, Zhuo-Hao Liu and Christopher E. G. Uff
Biomedicines 2022, 10(3), 518; https://doi.org/10.3390/biomedicines10030518 - 22 Feb 2022
Cited by 7 | Viewed by 4362
Abstract
Traumatic brain injury (TBI) is an extremely complex disease and current systems classifying TBI as mild, moderate, and severe often fail to capture this complexity. Neuroimaging cannot resolve the cellular and molecular changes due to lack of resolution, and post-mortem tissue examination may [...] Read more.
Traumatic brain injury (TBI) is an extremely complex disease and current systems classifying TBI as mild, moderate, and severe often fail to capture this complexity. Neuroimaging cannot resolve the cellular and molecular changes due to lack of resolution, and post-mortem tissue examination may not adequately represent acute disease. Therefore, we examined the cellular and molecular sequelae of TBI in fresh brain samples and related these to clinical outcomes. Brain biopsies, obtained shortly after injury from 25 living adult patients suffering severe TBI, underwent immunohistochemical analysis. There were no adverse events. Immunostaining revealed various qualitative cellular and biomolecular changes relating to neuronal injury, dendritic injury, neurovascular injury, and neuroinflammation, which we classified into 4 subgroups for each injury type using the newly devised Yip, Hasan and Uff (YHU) grading system. Based on the Glasgow Outcome Scale-Extended, a total YHU grade of ≤8 or ≥11 had a favourable and unfavourable outcome, respectively. Biomolecular changes observed in fresh brain samples enabled classification of this heterogeneous patient population into various injury severity categories based on the cellular and molecular pathophysiology according to the YHU grading system, which correlated with outcome. This is the first study investigating the acute biomolecular response to TBI. Full article
(This article belongs to the Special Issue Advances Research in Traumatic Encephalopathy)
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32 pages, 4656 KiB  
Article
Poloxamer 188 Exerts Direct Protective Effects on Mouse Brain Microvascular Endothelial Cells in an In Vitro Traumatic Brain Injury Model
by Felicia P. Lotze and Matthias L. Riess
Biomedicines 2021, 9(8), 1043; https://doi.org/10.3390/biomedicines9081043 - 19 Aug 2021
Cited by 9 | Viewed by 3405
Abstract
Traumatic Brain Injury (TBI), the main contributor to morbidity and mortality worldwide, can disrupt the cell membrane integrity of the vascular endothelial system, endangering blood–brain barrier function and threatening cellular subsistence. Protection of the vascular endothelial system might enhance clinical outcomes after TBI. [...] Read more.
Traumatic Brain Injury (TBI), the main contributor to morbidity and mortality worldwide, can disrupt the cell membrane integrity of the vascular endothelial system, endangering blood–brain barrier function and threatening cellular subsistence. Protection of the vascular endothelial system might enhance clinical outcomes after TBI. Poloxamer 188 (P188) has been shown to improve neuronal function after ischemia/reperfusion (I/R) injury as well as after TBI. We aimed to establish an in vitro compression-type TBI model, comparing mild-to-moderate and severe injury, to observe the direct effects of P188 on Mouse Brain Microvascular Endothelial Cells (MBEC). Confluent MBEC were exposed to normoxic or hypoxic conditions for either 5 or 15 h (hours). 1 h compression was added, and P188 was administered during 2 h reoxygenation. A direct effect of P188 on MBEC was tested by assessing cell number/viability, cytotoxicity/membrane damage, metabolic activity, and total nitric oxide production (tNOp). While P188 enhanced cell number/viability, metabolic activity, and tNOp, an increase in cytotoxicity/membrane damage after mild-to-moderate injury was prevented. In severely injured MBEC, P188 improved metabolic activity only. P188, present during reoxygenation, influenced MBEC function directly in simulated I/R and compression-type TBI. Full article
(This article belongs to the Special Issue Advances Research in Traumatic Encephalopathy)
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Review

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13 pages, 303 KiB  
Review
Chronic Traumatic Encephalopathy: Update on Current Clinical Diagnosis and Management
by Kevin Pierre, Kyle Dyson, Abeer Dagra, Eric Williams, Ken Porche and Brandon Lucke-Wold
Biomedicines 2021, 9(4), 415; https://doi.org/10.3390/biomedicines9040415 - 12 Apr 2021
Cited by 20 | Viewed by 8039
Abstract
Chronic traumatic encephalopathy is a disease afflicting individuals exposed to repetitive neurotrauma. Unfortunately, diagnosis is made by postmortem pathologic analysis, and treatment options are primarily symptomatic. In this clinical update, we review clinical and pathologic diagnostic criteria and recommended symptomatic treatments. We also [...] Read more.
Chronic traumatic encephalopathy is a disease afflicting individuals exposed to repetitive neurotrauma. Unfortunately, diagnosis is made by postmortem pathologic analysis, and treatment options are primarily symptomatic. In this clinical update, we review clinical and pathologic diagnostic criteria and recommended symptomatic treatments. We also review animal models and recent discoveries from pre-clinical studies. Furthermore, we highlight the recent advances in diagnosis using diffusor tensor imaging, functional magnetic resonance imaging, positron emission tomography, and the fluid biomarkers t-tau, sTREM2, CCL11, NFL, and GFAP. We also provide an update on emerging pharmaceutical treatments, including immunotherapies and those that target tau acetylation, tau phosphorylation, and inflammation. Lastly, we highlight the current literature gaps and guide future directions to further improve clinical diagnosis and management of patients suffering from this condition. Full article
(This article belongs to the Special Issue Advances Research in Traumatic Encephalopathy)
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