Caffeine Could Stave Off Multiple Sclerosis

June 30 (HealthDay News) -- Caffeine just might prevent multiple sclerosis, a new animal study suggests.

Giving mice the equivalent of 6 to 8 cups of coffee a day prevented mice from getting the animal model equivalent of MS, said Dr. Linda Thompson, of the Oklahoma Medical Research Foundation, and a member of the team reporting the finding in this week's issue of the Proceedings of the National Academy of Sciences.

Multiple sclerosis, an autoimmune disease, affects about 400,000 Americans, according to the National Multiple Sclerosis Society. The T-cells from the body's immune system attack the myelin, the fatty sheath that normally protects the nerve fibers in the central nervous system. This, in turn, produces scar tissue and triggers the symptoms of MS, which can include numbness, weakness, lack of muscle coordination and problems with bladder control, speech and vision.

Here's why the coffee warded off MS, Thompson explained: It prevented the molecule adenosine, one of the four building blocks of DNA, from binding to the adenosine receptor at the cellular level. When adenosine cannot bind to receptors at the cellular level, this in turn prevents T-cells from reaching the central nervous system and setting off the events that lead to the animal version of MS.

"From a scientific point of view, the bottom line is, adenosine in this mouse model is needed for the disease-causing T-cells to get into the central nervous system," Thompson said. "That was the big, unexpected finding."

The discovery shows how important the adenosine molecule is in allowing immune cells to infiltrate the central nervous system. In the animals, the T-cells were activated, but they couldn't get into the central nervous system, because the caffeine was bound to the adenosine receptors.

Dr. John Richert, executive vice president of research and clinical programs for the National Multiple Sclerosis Society, said the new finding is "potentially big news many years down the road."

But he cautioned that the research is in the early stages, and the whole process needs to be studied in humans.

Thompson agreed.

"First, we have to learn if adenosine plays the same role in people," she said. "In humans, it is not known if adenosine regulates the entry of T-cells into the central nervous system."

If the same findings bear out in humans, she said, the hope is to develop a drug that would degrade adenosine, prevent it from being formed, or prevent T-cells from getting into the central nervous system. She noted that the discovery holds promise for other autoimmune diseases, including lupus and rheumatoid arthritis.

The challenge, she said, is that adenosine receptors "are everywhere in the body." So, the drug would have to be specific enough to only act on the adenosine receptors that control access of the T-cells to the central nervous system.

Even so, Richert said, "it's a potential therapeutic target that needs to be explored."


SOURCES: Linda Thompson, Ph.D., member, Oklahoma Medical Research Foundation, Oklahoma City; John Richert, M.D., executive vice president, research and clinical programs, National Multiple Sclerosis Society, New York, N.Y.; June 30, 2008, Proceedings of the National Academy of Sciences
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