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Thymosin beta-4 in Multiple Sclerosis: Experimental Evidence for Regenerative Effects

While significant progress has been made in treating multiple sclerosis (MS) through immunomodulatory and anti-inflammatory therapies, regenerative strategies could provide an additional tool for addressing this chronic condition. Experimental research indicates that thymosin beta-4 (Tβ4) may support repair processes relevant to MS in both early and later stages of disease and could, in the future, be evaluated alone or in combination with existing therapies. Tβ4 has also improved functional outcomes in preclinical rodent models of embolic stroke (1) and traumatic brain injury (2).

In these models, Tβ4 increased myelinated axons and angiogenesis in the ischemic boundary and augmented remyelination. There was also an increase in oligodendrocyte progenitor cells and myelinating oligodendrocytes. The repair processes observed after stroke and trauma parallel those described in the heart after myocardial infarction, where Tβ4 promotes cardiomyocyte survival and improved cardiac function by recruiting stem/progenitor cells and reducing inflammation and scar formation (3). Tβ4 appears capable of modulating inflammatory processes in the brain, which opens avenues for eventual evaluation in a range of progressive and neurodegenerative conditions (4).

References

1. Morris DC, Chopp M, Zhang L, et al. Thymosin Tbeta4 improves functional neurological outcome in a rat model of embolic stroke. Neuroscience 2010;169:674-82.

2. Xiong Y, Mahmood A, Meng Y, et al. Treatment of traumatic brain injury with thymosin beta4 in rats. J Neurosurg 2011;114:102-15.

3. Bjørklund G, Dadar M, Aaseth J, Chirumbolo S. Thymosin β4: A Multi-Faceted Tissue Repair Stimulating Protein in Heart Injury. Curr Med Chem 2020;27:6294-305.

4. Pardon MC. Share Anti-inflammatory potential of thymosin β4 in the central nervous system: implications for progressive neurodegenerative diseases. Expert Opin Biol Ther 2018;18(sup1):165-9. doi: 10.1080/14712598.2018.1486817