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Editorial

Thymosin β4 as a restorative/regenerative therapy for neurological injury and neurodegenerative diseases

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Abstract

Thymosin β4 (Tβ4) promotes CNS and peripheral nervous system (PNS) plasticity and neurovascular remodeling leading to neurological recovery in a range of neurological diseases. Treatment of neural injury and neurodegenerative disease 24 h or more post-injury and disease onset with Tβ4 enhances angiogenesis, neurogenesis, neurite and axonal outgrowth, and oligodendrogenesis, and thereby, significantly improves functional and behavioral outcomes. We propose that oligodendrogenesis is a common link by which Tβ4 promotes recovery after neural injury and neurodegenerative disease. The ability to target many diverse restorative processes via multiple molecular pathways that drive oligodendrogenesis and neurovascular remodeling may be mediated by the ability of Tβ4 to alter cellular expression of microRNAs (miRNAs). However, further investigations on the essential role of miRNAs in regulating protein expression and the remarkable exosomal intercellular communication network via exosomes will likely provide insight into mechanisms of action and means to amplify the therapeutic effects of Tβ4.

Declaration of interest

This paper is part of a supplemental issue, sponsored by SciClone. The authors were supported by NIH, grant R01 AG037506 (MC) and R01 NS079612 (ZG). The authors are employees of Henry Ford Hospital, which has a Material Transfer Agreement with RegeneRx Biopharmaceuticals, Inc., Rockville, MD. A US Provisional Patent 61/163,556 has been filed for use of Tβ4 in neurological injury. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

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