Multiple Sclerosis is one of the biggest health puzzles left for medical science to solve. Researchers from the prestigious Stanford University School of Medicine have possibly put together another piece of it though. Preliminary studies, using both laboratory mice and human brain tissue seem to indicate there may be a link between Multiple Sclerosis and high blood pressure – and that an inexpensive drug that has been on the market for uses may indeed have some therapeutic value in the treatment of the disease.

One of the senior authors of the paper, Lawrence Steinman, MD got the idea for the line of research several years ago after he himself was diagnosed with high blood pressure and was started on the medication lisinopril by his physician. As he says he does with all medications he encounters he went home and did a quick Google search on lisinopril, just to make sure he understood what he was going to be taking.

Steinamn was already a noted Multiple Sclerosis researcher and perhaps because of the volume of work he has done on the subject he says that his computer had a glitch, it would insert the term Multiple Sclerosis to each and every internet search he performed on it.

When he searched for lisinopril he found that a number of medical articles popped up that to him seemed to suggest that there was a possible link between multiple sclerosis and a hormone angiotensin, which cause blood vessels to constrict in a response to a change in the body’s posture. Angiotensin over activity is one cause of hypertension and lisinopril acts upon it by blocking an enzyme that angiotensin’s precursor into the active hormone.

Steinman and his colleagues began testing the multiple sclerosis/angiotensin connection using the more advanced scientific techniques that were now available to them. In examining the brain samples of autopsied patients which displayed multiple sclerosis lesions they found elevated levels of both angiotensin and the associated enzyme that is blocked by lisinopril.

To further test their theories they used laboratory bred mice who had been injected with chemicals that induce brain lesions very similar to those of multiple sclerosis patients. When they were given lisinopril before being injected the mice didn’t develop paralysis characteristic of the diseases progression. But, if it was given after the mice developed full-blown symptoms, lisinopril seemingly reversed their paralysis.

In addition the researchers found that the lisinopril caused accelerated growth of regulatory T cells, which are essential to the body’s immune system.

For some the implications of the Steinman et al study are major. The current drug therapies for multiple sclerosis are hugely expensive while lisinopril is a relatively cheap drug. This could result in savings of tens of thousands of dollars in the costs of treating patients every year.

The study published online on Aug. 17 by the Proceedings of the National Academy of Sciences.

Steinmans results have major public health significances, says Marc Feldmann, an Imperial College London immunologist who is well-versed with the study but didn’t take part in it. He mentioned that these therapies for multiple sclerosis (including Tysabri) are costly monoclonal antibodies, costing tens of thousands of dollars each year for every patient treated. If we can treat multiple-sclerosis patients with lisinopril at about 1 percent of the price of Tysabri treatment, then many more patients will receive enough therapy, at a substantially cheaper price to those paying for it,  Feldmann said.

First writing of the paper is shared by two postdoc researchers in Steinman’s lab: Michael Platten, MD, and Sawsan Youssef, PhD. (Platten is a professor of neurology now at University Hospital of Heidelberg, in Germany.) Other Stanford writers include May Han, MD and acting assistant professor of neurology and neurological sciences and Raymond Sobel, MD professor of pathology.

The research was funded by the National Institutes of Health, the National MS Society, the Phil N. Allen Trust, the German Research Foundation, the Helmholtz Association, the U.S. Public Health Service and the Biomedical Sciences Exchange Program.