New use for old multiple sclerosis drug shows great promise for a cure
- Almost a million people in the U.S. and about 2.8 million people worldwide live with multiple sclerosis.
- Research is indicating interferon beta could offer a potential new path to treatment.
- The drug is already in use for multiple sclerosis treatment.
Multiple sclerosis (MS) is a debilitating disease that causes pain, numbness and mobility issues that worsen over time. Unfortunately, it is also quite common.
According to the National Multiple Sclerosis Society, almost a million people in the U.S. and about 2.8 million people worldwide live with MS. So, how do people and healthcare experts tackle this disorder?
Uses of interferon betas
This disease damages the myelin sheath, an insulating layer of proteins and fats wrapped around nerves, which leads to impaired neuronal signaling and is commonly treated by drugs called interferon betas.
These powerful drugs reduce relapses and slow motor function decline. They achieve this by getting interferon beta, a protein known to contain a zinc binding pocket, to reduce proinflammatory molecules and even increase the production of anti-inflammatory species. Now, new research, acquired by IE and released today, is indicating that the molecule reduces the binding of three components — zinc, C-peptide, and albumin — to red blood cells. This may offer new paths to using the same old drug for MS treatment.
“Cells that make myelin are sensitive to adenosine triphosphate (ATP) and nitric oxide (NO), molecules that are present in high amounts in the blood and brain lesions of MS patients. Red blood cells can release NO directly, but they can also stimulate NO production in the lining of blood vessels by releasing ATP. NO can then go on to damage nerves in MS patients. Zinc, C-peptide — which is secreted by the pancreas along with insulin — and albumin are key players in the latter process, and they can latch onto red blood cells,” explained the researchers.
Sopping up zinc
The scientists further speculated that because interferon beta can bind zinc, it may just be useful to MS patients by sopping up this mineral. Dana Spence, professor of biomedical engineering and chemistry at Michigan State University, and a team of colleagues decided to investigate this possibility by conducting lab tests. What they found was nothing short of impressive.
“Red blood cells from MS patients bound more zinc, C-peptide and albumin than cells from control subjects. Treatment with interferon beta reduced this interaction in MS samples down to control levels. Albumin boosted zinc and C-peptide binding to MS red blood cells, and this effect went away with interferon beta treatment,” reported the researchers in their statement.
The conclusion from this study was that it’s likely that the drug is inhibiting albumin binding, keeping it from delivering its cargo of C-peptide and zinc to red blood cells so that NO can be made. This development could produce a new cure for MS one that is viable and easily tolerated by patients.
The research was published in ACS Chemical Neuroscience.
Multiple sclerosis (MS) is an inflammatory disease characterized by damage to the myelin sheath surrounding axons in the central nervous system. While the exact mechanism of this destruction is unknown, excess nitric oxide (NO) and adenosine triphosphate (ATP) have been measured in tissues and liquids obtained from people with MS. Here, incubation of interferon-beta (IFN-β), an MS drug with an unknown mechanism of action, with red blood cells (RBCs) obtained from people with MS provide evidence of a potential hypermetabolic state in the MS RBC that is decreased with IFN-β intervention. Specifically,binding of all three components of an albumin/C-peptide/Zn complex to MS RBCs was significantly increased in comparison to control RBCs. For example, the binding of C-peptide to MS RBCs was significantly increased (3.4 ± 0.1 nM) compared to control RBCs (1.6 ± 0.2 nM). However, C-peptide binding to MS RBCs was reduced to a value (1.6 ± 0.3 nM) statistically equal to that of control RBCs in the presence of 2 nM IFN-β. Similar trends were measured for albumin and Zn binding to RBCs when in the presence of IFN- β. RBC function was also affected by incubation of cells with IFN-β. Specifically, RBC-derived ATP and measurable membrane GLUT1 were both significantly decreased (56 and 24%, respectively) in the presence of IFN-β. Collectively, our results suggest that IFN-β inhibits albumin binding to the RBC, thereby reducing its ability to deliver ligands such as C-peptide and Zn to the cell and normalizing the basal hypermetabolic state.
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