Volume 1270, Issue 1 p. 51-58

Neuroprotective and neurorestorative effects of thymosin β4 treatment following experimental traumatic brain injury

Ye Xiong

Ye Xiong

Departments of Neurosurgery, Henry Ford Health System, Detroit, Michigan.

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Asim Mahmood

Asim Mahmood

Departments of Neurosurgery, Henry Ford Health System, Detroit, Michigan.

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Yuling Meng

Yuling Meng

Departments of Neurosurgery, Henry Ford Health System, Detroit, Michigan.

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Yanlu Zhang

Yanlu Zhang

Departments of Neurosurgery, Henry Ford Health System, Detroit, Michigan.

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Zheng Gang Zhang

Zheng Gang Zhang

Neurology, Henry Ford Health System, Detroit, Michigan.

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Daniel C. Morris

Daniel C. Morris

Emergency Medicine, Henry Ford Health System, Detroit, Michigan.

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Michael Chopp

Michael Chopp

Neurology, Henry Ford Health System, Detroit, Michigan.

Department of Physics, Oakland University, Rochester, Michigan

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First published: 10 October 2012
Citations: 37
Ye Xiong, M.D., Ph.D., Henry Ford Health System, Department of Neurosurgery, E&R Building, Room # 3096, 2799 West Grand Boulevard, Detroit, MI 48202. [email protected]

Abstract

Traumatic brain injury (TBI) remains a leading cause of mortality and morbidity worldwide. No effective pharmacological treatments are available for TBI because all phase II/III TBI clinical trials have failed. This highlights a compelling need to develop effective treatments for TBI. Endogenous neurorestoration occurs in the brain after TBI, including angiogenesis, neurogenesis, synaptogenesis, oligodendrogenesis, and axonal remodeling, which may be associated with spontaneous functional recovery after TBI. However, the endogenous neurorestoration following TBI is limited. Treatments amplifying these neurorestorative processes may promote functional recovery after TBI. Thymosin beta 4 (Tβ4) is the major G-actin–sequestering molecule in eukaryotic cells. In addition, Tβ4 has other properties including antiapoptosis and anti-inflammation, promotion of angiogenesis, wound healing, stem/progenitor cell differentiation, and cell migration and survival, which provide the scientific foundation for the corneal, dermal, and cardiac wound repair multicenter clinical trials. Here, we describe Tβ4 as a neuroprotective and neurorestorative candidate for treatment of TBI.