People who suffer from brain or spinal cord trauma often have few options beyond physical therapy and hope; injuries to the central nervous system rarely heal and often worsen over time.

But recently, researchers from Helsinki, Finland, found a tiny chunk of protein that not only keeps these cells alive but also encourages new cells to grow.

The protein—called KDI tri-peptide (KDI)—could someday lead to new treatment options for people suffering from a wide range of neurological problems from spinal cord injury to Alzheimer's disease, says researcher Päivi Liesi. In earlier studies, Liesi and her colleagues found that rats with damaged spinal cords could walk again after three months when they injected KDI near the injury. The protein also shows promise for human cells, at least in the petri dish.

How does KDI work? Liesi's most recent research, which appeared July 25 on the Journal of Neuroscience Research website, found that the KDI protein prevents cell death by blocking a substance called glutamate. Normally, glutamate helps cells communicate with one another for learning and memory. However, glutamate is toxic to injured neural cells, causing the cells to take in too much calcium and die. This cell death by glutamate occurs in many different types of nervous system injuries and diseases, including Alzheimer's disease, Lou Gehrig's disease, and spinal cord injuries.

According to Liesi, the most recent drugs used to treat neurological disease inhibit, to some degree, the effect of glutamate. What makes KDI unique is its ability to block three major types of glutamate receptors on the cell surface. In one test, KDI eliminated around 90 percent of glutamate's effect on human brain cells.

Further, KDI should prove nontoxic to humans. KDI is one part of a larger protein called laminin that occurs naturally in the human body. Provided the clinical trials on KDI go well (they could start in 2006), it may take less time for the Food and Drug Administration to approve the drug for use in humans than the 10 or more years it takes most drugs.

The effect of KDI that Liesi describes is not unlike those discovered in similar studies using stem cells. In 2004, researchers from Johns Hopkins found that stem cells, when injected near the injured peripheral nerves of rats, cause the nerves to heal and grow. The researchers say the stem cells did not turn into nerve cells but most likely secreted some substance that encouraged the damaged cells to recuperate.

"They are usually considered molecules that are involved in development," says Liesi of the laminin proteins. "My belief is that it not only works against the glutamate but that it also has its own beneficial functions that are related to its ability to promote neuron growth."

Researchers in the United States say the study of KDI proteins is preliminary and that more tests are needed to confirm the protein's effects. Dr. Rick Huganir, professor of neuroscience at the Johns Hopkins School of Medicine and an investigator with the Howard Hughes Medical Institute, says the test wasn't as clear as it could have been and that the protein could affect receptors that have nothing to do with glutamate.

"The problem I have with [KDI] is that it had similar effects on most of the receptors they tried," he explains.

Liesi acknowledges that more work is needed.

"So far things have been amazingly good," she says. "However, a human is still different from an animal."

For more information: The U.S. National Library of Medicine and the National Institutes of Health have a good website on neurological disorders.