Lawrence SteinmanThe latest study from the Stanford University School of Medicine claims that there is a connection between mice and human brain tissue, which is apparently between high blood pressure and multiple sclerosis. The study suggests that for multiple sclerosis the same drug may have therapeutic value which is already a safe and economical drug for blood pressure.

Lawrence Steinman, MD senior author of the research however warns that to decide whether the drug which is known as lisinopril has the same effect on humans as it has on mice extensive clinical trial work is necessary.

Lawrence Steinman eagerly states “We were able to show that all the targets for lisinopril are there and ready for therapeutic manipulation in the multiple-sclerosis lesions of human patients. Without that, this would be just another intriguing paper about what’s possible in the mouse.”

Seven years ago Steinman reveals that he had blood pressure. Lisinopril, a drug which is known for its safety and used by thousands of people was administered to him by his doctor. Annoyed, Steinman did a Google search on the drug. Steinman is known to be a prominent multiple Sclerosis researcher. He has already worked on the inflammatory features of the disease which stimulated growth of a chartbuster class of anti-inflammatory multiple-sclerosis therapeutics. One of the drugs that were promoted under the trade name Tysabri was the drug natalizumab.

A fault sneaked in Steinman’s home computer, apparently whenever he typed in any keyword into a search site, this term ‘multiple sclerosis’ involuntarily popped up. This to his astonishment gave out an unclear possible relation that was apparently seen between multiple sclerosis and a fast acting angiotensin, as the medical literature which popped up presented hints. This hormone’s receptors thrive on blood-vessel walls all over the body. If there is a shift in posture then angiotensin instantaneously causes blood vessels to compress.

Steinman, who is also the George A. Zimmerman Professor in the medical school states, “That raises your blood pressure so when you stand up to get out of a chair, you don’t fall down and faint,”

Chronic hypertension seems to be caused by over action of angiotensin. The blood pressure is controlled by Lisinopril by blocking an enzyme that switches angiotensin’s precursor into the active hormone. A few anti-inflammatory properties were apparently seen in the drug. Multiple sclerosis is actually a chronic and sometimes deadly autoimmune disease in which the body’s immune system accumulates persisting assaults on the myelin casing of nerve cells in the brain. Due to this nerves supposedly malfunction which can result in blindness and paralysis. The inflammatory process is apparently due to multiple sclerosis and atherosclerosis.

Modern scientific techniques were then used by Steinman and his colleagues to examine the association between angiotensin/multiple –sclerosis. From autopsied patients multiple sclerosis of brain samples were checked. In those lesions, well recognized molecular-detection methods increased remarkably high levels of both the angiotensin receptor and the angiotensin-producing enzyme which was blocked by lisinopril.

The experts experimented on a laboratory mouse and after it was immunized with a certain chemical, it developed brain lesions that were akin to those observed in multiple sclerosis. Apparently before they were immunized with the chemical that activates the disease, the mice were given the same dosage of lisinopril that humans are given for high blood pressure. It was observed that due to this they did not develop paralysis. Lisinopril supposedly reversed their paralysis if it was administered after the mice developed full-blown symptoms.

Apparently it was seen that lisonopril administration decreased several molecular measures of inflammation that escort multiple sclerosis in humans and it’s analog in the animal model. Supposedly the mice’s overall immune competence was not withdrawn by the drug.

Adding to it was that lisinopril administration activated the increase of a significant class of immune cells which were called Regulatory T cells that avert autoimmune diseases by dialing down the action of other immune cells incorrectly aiming cells and tissues that should be left alone. Steinman is of the opinion that this rise was the main part in the defense supplied by the drug, as a combination of regulatory T cells from mice that had been provided lisinopril was adequate to avert or reverse the disease process in mice that had been given none.

Marc Feldmann, an Imperial College London immunologist who is aware of the study but did not take part in it had stated “If multiple-sclerosis patients can be treated with lisinopril at something like 1 percent of the price of treatment with Tysabri, then far more patients will receive adequate therapy, at a substantially lower cost to those paying for it”.

Feldmann is of the opinion that Steinman’s results would have major public-health connotations. He noted that the present therapies used for treating multiple sclerosis (including Tysabri) are very pricey and expensive and costs tens of thousands of dollars yearly for a single patient to be treated. The antibodies are extremely expensive.

This study was published online by the Proceedings of the National Academy of Sciences.