Traumatic Brain Injury and Stem Cell: Pathophysiology and Update on Recent Treatment Modalities
Traumatic brain injury (TBI) is a complex condition that presents with a wide spectrum of clinical symptoms caused by an initial insult to the brain through an external mechanical force to the skull. In the United States alone, TBI accounts for more than 50,000 deaths per year and is one of the lead...
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Format: | Article |
Language: | English |
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Wiley
2017-01-01
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Series: | Stem Cells International |
Online Access: | http://dx.doi.org/10.1155/2017/6392592 |
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author | Cesar Reis Vadim Gospodarev Haley Reis Michael Wilkinson Josileide Gaio Camila Araujo Sheng Chen John H. Zhang |
author_facet | Cesar Reis Vadim Gospodarev Haley Reis Michael Wilkinson Josileide Gaio Camila Araujo Sheng Chen John H. Zhang |
author_sort | Cesar Reis |
collection | DOAJ |
description | Traumatic brain injury (TBI) is a complex condition that presents with a wide spectrum of clinical symptoms caused by an initial insult to the brain through an external mechanical force to the skull. In the United States alone, TBI accounts for more than 50,000 deaths per year and is one of the leading causes of mortality among young adults in the developed world. Pathophysiology of TBI is complex and consists of acute and delayed injury. In the acute phase, brain tissue destroyed upon impact includes neurons, glia, and endothelial cells, the latter of which makes up the blood-brain barrier. In the delayed phase, “toxins” released from damaged cells set off cascades in neighboring cells eventually leading to exacerbation of primary injury. As researches further explore pathophysiology and molecular mechanisms underlying this debilitating condition, numerous potential therapeutic strategies, especially those involving stem cells, are emerging to improve recovery and possibly reverse damage. In addition to elucidating the most recent advances in the understanding of TBI pathophysiology, this review explores two primary pathways currently under investigation and are thought to yield the most viable therapeutic approach for treatment of TBI: manipulation of endogenous neural cell response and administration of exogenous stem cell therapy. |
format | Article |
id | doaj-art-9dc5a23c3b3941bcb4709bb348265bc4 |
institution | Kabale University |
issn | 1687-966X 1687-9678 |
language | English |
publishDate | 2017-01-01 |
publisher | Wiley |
record_format | Article |
series | Stem Cells International |
spelling | doaj-art-9dc5a23c3b3941bcb4709bb348265bc42025-02-03T01:22:29ZengWileyStem Cells International1687-966X1687-96782017-01-01201710.1155/2017/63925926392592Traumatic Brain Injury and Stem Cell: Pathophysiology and Update on Recent Treatment ModalitiesCesar Reis0Vadim Gospodarev1Haley Reis2Michael Wilkinson3Josileide Gaio4Camila Araujo5Sheng Chen6John H. Zhang7Department of Physiology and Pharmacology, Loma Linda University School of Medicine, 11041 Campus Street, Risley Hall, Room 219, Loma Linda, CA 92354, USADepartment of Physiology and Pharmacology, Loma Linda University School of Medicine, 11041 Campus Street, Risley Hall, Room 219, Loma Linda, CA 92354, USALoma Linda University School of Medicine, Loma Linda, CA 92354, USALoma Linda University School of Medicine, Loma Linda, CA 92354, USADepartment of Epidemiology & Biostatistics, Loma Linda School of Public Health, Loma Linda, CA 92350, USADepartment of Physiology and Pharmacology, Loma Linda University School of Medicine, 11041 Campus Street, Risley Hall, Room 219, Loma Linda, CA 92354, USADepartment of Neurosurgery, Second Affiliated Hospital School of Medicine, Zhejiang University, Hangzhou, ChinaDepartment of Physiology and Pharmacology, Loma Linda University School of Medicine, 11041 Campus Street, Risley Hall, Room 219, Loma Linda, CA 92354, USATraumatic brain injury (TBI) is a complex condition that presents with a wide spectrum of clinical symptoms caused by an initial insult to the brain through an external mechanical force to the skull. In the United States alone, TBI accounts for more than 50,000 deaths per year and is one of the leading causes of mortality among young adults in the developed world. Pathophysiology of TBI is complex and consists of acute and delayed injury. In the acute phase, brain tissue destroyed upon impact includes neurons, glia, and endothelial cells, the latter of which makes up the blood-brain barrier. In the delayed phase, “toxins” released from damaged cells set off cascades in neighboring cells eventually leading to exacerbation of primary injury. As researches further explore pathophysiology and molecular mechanisms underlying this debilitating condition, numerous potential therapeutic strategies, especially those involving stem cells, are emerging to improve recovery and possibly reverse damage. In addition to elucidating the most recent advances in the understanding of TBI pathophysiology, this review explores two primary pathways currently under investigation and are thought to yield the most viable therapeutic approach for treatment of TBI: manipulation of endogenous neural cell response and administration of exogenous stem cell therapy.http://dx.doi.org/10.1155/2017/6392592 |
spellingShingle | Cesar Reis Vadim Gospodarev Haley Reis Michael Wilkinson Josileide Gaio Camila Araujo Sheng Chen John H. Zhang Traumatic Brain Injury and Stem Cell: Pathophysiology and Update on Recent Treatment Modalities Stem Cells International |
title | Traumatic Brain Injury and Stem Cell: Pathophysiology and Update on Recent Treatment Modalities |
title_full | Traumatic Brain Injury and Stem Cell: Pathophysiology and Update on Recent Treatment Modalities |
title_fullStr | Traumatic Brain Injury and Stem Cell: Pathophysiology and Update on Recent Treatment Modalities |
title_full_unstemmed | Traumatic Brain Injury and Stem Cell: Pathophysiology and Update on Recent Treatment Modalities |
title_short | Traumatic Brain Injury and Stem Cell: Pathophysiology and Update on Recent Treatment Modalities |
title_sort | traumatic brain injury and stem cell pathophysiology and update on recent treatment modalities |
url | http://dx.doi.org/10.1155/2017/6392592 |
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