Medical researchers have made a significant advance in understanding multiple sclerosis, a common neurological disease that causes symptoms ranging from muscle weakness to paralysis.

The disease is one in which the body’s immune system mistakenly attacks the electrical insulation of nerve fibers. The cause is part genetic and part environmental, but researchers trying to identify the relevant genes have endured repeated frustration. Their approach has been to guess what genes might be involved and see if patients have abnormal versions.

This guesswork has produced more than 100 candidate genes in recent years, none of which could be confirmed except for long-known variants in the mechanism used by the immune system to recognize proteins that are foreign to the body.

In three articles published online yesterday in The New England Journal of Medicine, three teams of researchers say they have identified, by separate routes, new genetic variants that contribute to the disease.

One team used a new, advanced gene-hunting method called Whole Genome Association, which has racked up a string of successes with major diseases in the last few months. The other teams used the candidate gene approach, but because all three teams identified the same gene, the researchers say they are confident they have opened a new window into the cause and possible treatment of multiple sclerosis.

The gene makes a substance called the interleukin-7 receptor, a protein that enables cells of the immune system to respond to a control agent. Researchers believe the receptor is part of a biochemical pathway involving many genes; defects in any of these genes may lead to the disease. It is now possible to explore the pathway, they say, in the hope of devising treatments to correct the disease-causing process.

The new research is the product of several large teams at universities in the United States and abroad who have coordinated their publications and pooled their data for analysis.

The leaders of the Whole Genome Association Study include David A. Hafler of Brigham and Women’s Hospital in Boston; Stephen L. Hauser of the University of California, San Francisco; and Jonathan L. Haines of Vanderbilt University Medical Center in Nashville. The two candidate gene studies were headed by Dr. Haines and Jan Hillert of the Karolinska Institute in Stockholm.

Because the course of the disease is unpredictable, clinical trials are hard to conduct, said Dr. Kári Stefánsson, chief executive of Decode Genetics in Reykjavik, Iceland. “But once you have an ironclad discovery, as I believe the interleukin-7 receptor is,” Dr. Stefánsson said, “then you have the motivation to endure the expense of a long clinical trial.”

The full list of principal investigators participating in the Whole Genome Association study is as follows: David A. Hafler of the Brigham and Women’s Hospital; Eric S. Lander and John D. Rioux of the Broad Institute and Massachusetts Institute of Technology; Stephen L. Hauser and Jorge R. Oksenberg of the University of California, San Francisco, Alastair Compston and Stephen Sawcer of the University of Cambridge School of Clinical Medicine; Margaret A. Pericak-Vance of the University of Miami School of Medicine and Jonathan L. Haines of the Vanderbilt University Medical Center.