An American pharmaceutical company claims to be developing a process that has promoted remyelination in two animal models ‘commonly used’ for multiple sclerosis research. Details of the process using Thymosin beta4, which is a protein that occurs naturally in the human body, were published in Neurobiology of Disease.
RegenRx Biopharmaceuticals Inc, based in the US state of Maryland, is a clinical-stage drug development company concentrating on tissue protection, repair and regeneration. It believes Thymosin could be developed as a therapy for multiple sclerosis and other demyelinating neurological disorders.
I suspect few but the most determined people would persevere when faced with an article headed, and I kid you not, Thymosin beta4 promotes oligodendrogenesis in the demyelinating central nervous system.
Ok, well, let’s just say some of us are made of stronger stuff than others. That is my excuse and no going back now.
Now, all of us who have MS know that our illness is the result of our immune systems attacking and damaging the myelin that protects our nerves, rather like the rubber that surrounds electric wires. For the more technical, myelin is a lipidic material that protects the nerve fibres in the central and peripheral nervous systems.
Now that long word in the scientific title comes from the fact that myelination, the process of myelin formation around neurons, is carried out by things called oligodendrocytes in the central nervous system. The article says: “These mature cells do not have the capacity to replicate, so once they are destroyed the only way to reinitiate myelination would be to recruit or generate oligodendrocyte progenitor cells (OPCs). These precursor cells may then proliferate and differentiate into myelin-producing mature oligodendrocytes.”
As I said above, destruction of the protective myelin is what MS is all about. It leads to the slowing down and even failure of messages being sent through the nervous system – something that researchers and doctors call progressive neurodegeneration and synaptic failure.
Despite the existence of several disease modifying medications (DMDs), at present there is no effective remyelination therapy.
Researchers from the Departments of Neurology and Biostatistics and Research Epidemiology, Henry Ford Health System in Detroit, and from the Department of Physics at Oakland University in Rochester, worked on the project.
They demonstrated that: ‘Thymosin beta4 (Tβ4) is an effective remyelination therapy, able to promote proliferation and differentiation of OPCs into mature, myelin-producing oligodendrocytes, while also decreasing axonal damage.’ The research team also observed that the epidermal growth factor receptor (EGFR) contributes to the process.
Two animal models widely used in MS research were used in the evaluation stages. These were the experimental autoimmune encephalomyelitis (EAE) and the cuprizone diet models. Both showed: ‘the improved rate of remyelination and mature oligodendrocytes generation significantly correlated with functional improvement in the mice.’
The researchers concluded these findings of this pre-clinical trial indicate that:
1) Tβ4 increases proliferation of OPCs and the maturation of OPCs to myelinating oligodendrocytes which in concert, likely contribute to the beneficial effect of Tβ4;
2) Epidermal Growth Factor Receptor upregulated and activated by Tβ4 may mediate the process of OPC differentiation;
3) Tβ4 could potentially be developed as a therapy for MS patients, and for other demyelinating neurological disorders.