Neuroprotective and neurorestorative effects of thymosin β4 treatment following experimental traumatic brain injury.
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.
Departments of Neurosurgery, Henry Ford Health System, Detroit, Michigan 48202, USA. yxiong1@hfhs.org
Ye
Y
Xiong
Asim
A
Mahmood
Yuling
Y
Meng
Yanlu
Y
Zhang
Zheng Gang
ZG
Zhang
Daniel C
DC
Morris
Michael
M
Chopp
D000818:Animals; D001930:Brain Injuries / Q000188:drug therapy*; D006801:Humans; D018919:Neovascularization, Physiologic / Q000187:drug effects; D055495:Neurogenesis / Q000187:drug effects; D051381:Rats; D013947:Thymosin / Q000627:therapeutic use*; D014945:Wound Healing / Q000187:drug effects; D000099201:Thymosin beta(4)
D013947:Thymosin; D000099201:Thymosin beta(4)