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Blood Pressure Drug Saves Myelin in Multiple Sclerosis

blood pressure drug saves myelin in multiple sclerosis

A new study showed that a drug used to treat high blood pressure prevented the loss of myelin in multiple sclerosis animal models. The blood pressure drug, called guanabenz (Wytensin), also reduced clinical symptoms of the disease.


Guanabenz is an alpha-2 adrenergic agonist that works by controlling how nerve signals move along certain pathways. This in turn relaxes the blood vessels so blood can flow more easily and blood pressure declines. Its most common side effects are dry mouth, drowsiness, dizziness, weakness, and headache, all occurring in more than 5 percent of users.

In another recent study, a research team reported on how a drug used to treat overactive bladder (solifenacin; Vesacare) appeared to be helpful in restoring myelin in multiple sclerosis. This new study, however, looks at a drug that may prevent myelin loss in the first place.

The team, under direction of senior author Brian Popko, PhD, Jack Miller Professor of Neurological Disorders at the University of Chicago, built on some of their previous research. They had noted that the brain cells (oligodendrocytes) responsible for myelin production die, increasing demyelination (myelin loss), in the presence of significant stress such as chronic inflammation, a hallmark of multiple sclerosis.

Other research had shown that guanabenz might help with this stress response. So Popko’s team conducted a set of four experiments.

Four experiments
The first one involved inducing inflammation in oligodendrocyte cells and then treating them with guanabenz. The result was prevention of myelin loss and restoration of cell survival to nearly normal levels.

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After that experiment, the team administered the blood pressure drug to mouse models of multiple sclerosis. Treated mice kept several times more myelination and oligodendrocytes than mice who were not treated.

In the third experiment, the scientists triggered an immune response against myelin in mice, simulating a chronic model of MS similar to that in humans. Guanabenz was then administered one week later, and although symptoms developed, the drug significantly delayed their onset and reduced their severity. Twenty percent of the mice did not develop any MS symptoms.

Finally, guanabenz was given to mice who already had symptoms of relapsing-remitting multiple sclerosis. The drug was administered immediately after symptoms peaked, and they declined by nearly 50 percent in severity during the next relapse event.

The authors concluded that guanabenz works in multiple sclerosis models by temporarily stopping reactivation of eukaryotic translation initiation factor 2 (eIF2a), a protein which, when deactivated, results in extended protection against cell death. Therefore, guanabenz use results in the death of fewer oligodendrocytes and a reduced inflammatory response, thus helping save myelin.

One hitch in the findings is that eIF2a reactivates after some time via a route that the blood pressure drug does not affect, which means the benefit does not continue. However, the researchers noted that their findings “provide support for guanabenz as the first oligodendrocyte-protective agent for the alleviation of inflammatory-mediated demyelination in diseases such as MS.”

Also read about alternative treatments for multiple sclerosis

Mayo Clinic, guanabenz
Way SW et al. Pharmaceutical integrated stress response enhancement protects oligodendrocytes and provides a potential multiple sclerosis therapeutic. Nature Communications 2015 Mar. doi:10.1038/ncomms7532