Two international research meetings.

This fall, the Americas Committee for Treatment and Research in MS gathered in Chicago and the European Committee for Treatment and Research in MS met in Madrid. Both ACTRIMS and ECTRIMS drew participants from around the world freely sharing data--showing again that the effort to derail MS is global.

* A number of EGTRIMS presentations focused on the disease-modifying drugs.

* A new formulation of Rebif was designed to reduce development of the neutralizing antibodies that can blunt the punch of interferons. The new version cut them almost in half and also slashed injection site reactions from 83.8% to 23.3%. This is from the first year of a two-year study involving 260 volunteers with MS. The new formulation is being reviewed by the FDA.

* Additional data from a trial with 942 volunteers who received Tysabri or a placebo infusion affirmed earlier good outcomes. Tysabri reduced relapses, progression of disability, and brain lesions seen on MRI. Tysabri also did well reducing the risk of worsening cognitive function (problems with concentration, memory, decisionmaking, and the like).

* A short course of Novantrone before beginning regular Copaxone therapy proved to be both safe and notably more effective than Copaxone alone, in a trial involving 40 people over 15 months.

* Finally, a 10-year follow-up study of Betaseron in secondary-progressive MS illustrated a familiar problem. Just 239 of the original 718 volunteers could be found. Only 85 were still on the drug. There was some good news nevertheless. People given the real drug during the first three years of the trial showed less progression than those who received inactive placebo injections.

On the other side of the Atlantic, ACTRIMS focused on the search for biomarkers, or easy-to-read signs to diagnose MS or track the impact of treatment.

* Proteins or genes? Some ACTRIMS researchers look to fields called genomics and proteomics. For example, one group looked at the immune system changes induced by Copaxone in order to identify genes that act differently in people who responded well as contrasted to those who did poorly. Preliminary findings suggest that a gene involved in producing an immune-signaling molecule (IL-18) may distinguish responders from those who get little benefit.

* MRI still rules. This non-invasive scan is the best "marker" to date--and techniques advance yearly. A Canadian group reported on an abnormally reduced signal called "Black T2" associated with losses of physical ability in MS. A larger study is now needed.