Oligodendrocytes are key neural cells responsible for producing myelin sheaths that wrap around neuronal axons in the central nervous system[1]. Considering that thymosin β4’s (Tβ4) ability to promote neurological recovery in a range of neurological diseases has been well established, Chopp & Zhang (2015) propose oligodendrogenesis as the common link by which Tβ4 supports and promotes recovery after neural injury and neurodegenerative disease.

Citing Tβ4’s propensity to alter cellular expression and target multiple molecular pathways involved in neurovascular remodeling and oligodendrogenesis, it warrants further study into Tβ4 as a restorative/regenerative therapy for neurological injury and neurodegenerative diseases.

Traditional treatment of neurological diseases, including stroke, traumatic brain injury (TBI), and multiple sclerosis have typically focused on the reduction of lesions and produced no effective or beneficial long-term therapeutic outcomes. As a result, new proposals suggest renewed focus on therapeutic efforts designed to facilitate the restorative process present after injury and with specific focus on the enhancement of neurovascular recovery resulting in improved neurological recovery.

Among the many benefits of using Tβ4 in the restorative/regenerative therapeutic process is that, unlike neuroprotection treatments that must be introduced to damaged tissue before irreversible damage occurs, this treatment can be administered several days – even weeks – after injury and still stimulate the naturally-occurring regenerative process that has been demonstrated to be beneficial in treating several conditions, including stroke and TBI.

Specifically, Tβ4 promotes the remodeling and restoration of the CNS/PNS post-injury and has been shown to improve neurological recovery by allowing for improved neurovascular plasticity, neurite outgrowth, myelination of axons, as well as increasing the production and release of trophic factors to further support the remodeling of the nervous system.

Multiple animal models have demonstrated that Tβ4 facilitates the restorative neurological process by simulating oligodendrocytes (OLGs) and specifically OLG progenitor cells (OPCs) in the CNS. It appears that Tβ4 expedited multiple pathways of neurological recovery by stimulating tiny non-coding RNAs known as microRNAs to promote the generation, translation, and differential of OPCs and OLGs.

While these findings are promising, what remains yet unknown is specifically how Tβ4 affects, or perhaps more appropriately, influences, microRNAs to communicate specific neurological restorative and regenerative instructions among various cells. The predominant theory emerging from relevant research is that this process of intercellular communication is created and moderated by tiny lipid particles known as exosomes. 

Considering the safety of Tβ4 for use in human trials and the potential for Tβ4 to treat neurological injury and degeneration, future clinical trials focusing on Tβ4’s specific influence on exosomes, and as a therapeutic restorative for neurological treatment and regeneration, is thought to hold promising clinical translation for future treatments of neurological disease and injury.

Source: (2015, January 22). Thymosin β4 as a restorative/regenerative therapy for …. Retrieved January 5, 2021, from https://www.tandfonline.com/doi/full/10.1517/14712598.2015.1005596


[1] (2015, October 15). Neuroinflammatory modulators of oligodendrogenesis. Retrieved January 2, 2021, from https://nnjournal.net/article/view/1129

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