After ringing in 2009, it’s worth noting that MS research may be disparate, but it doesn’t appear to be desperate as vastly different avenues of research are elucidating new approaches to disease evaluation and treatment.
In the last several months, the International Pediatric Multiple Sclerosis Study Group under the direction of Dale and Pillai in Australia has made an important distinction concerning demyelinating disease in the investigation of children. The researchers found that the biomarker oligoclonal bands (specific antibodies found in the spinal fluid, CSF) of children who have a Clinically Isolated Syndrome (for example an attack of optic neuritis and numbness on one side of the body or one of such problems alone) along with an MS consistent MRI were far more likely to go on to develop definite MS by having future clinical events compared to a group who did not fulfill the oligoclonal band-MRI criteria yet had a single demyelinating syndrome. This latter presentation has been called Acute Disseminated Encephalomyelitis (ADEM). Encephalopathy means an alteration in consciousness such as lowered alertness with confusion or delirium. When that change in mental status exists along with other features of what may seem like MS, there is a significantly less chance that the child will go on to develop MS.
CSF oligoclonal banding, an antibody biomarker for MS is often present in children (and adults) with the disease while it is often absent in those with ADEM.
Quintana this month published an even more specific biomarker analysis for MS patients than the longstanding oligoclonal bands. His group at Harvard looked at antigen microarrays identifying unique serum autoantibody signatures in subtypes of MS. Microarray analysis characterizes patterns of antibody reactivity in the blood of MS patients based on antibody coupling with certain antigens (biological proteins). Not only could the antibody panel for MS help distinguish MS from other neurological diseases such as Lupus, Adrenoleukodystrophy and Alzheimer disease, but the various MS subtypes could be sorted out based on what autoantibodies were present. For example, the commonly present Relapsing Remitting MS had autoantibodies different from either primary or secondary progressive MS subtypes. The use of this microarray technique holds a great deal of promise in helping to clarify disease progression potential in various MS patients and in clarifying whether or not MS exists in certain very difficult cases that might suggest an alternative diagnosis based on the work-up results.
Finally, not many of you have spent post-New Year’s Eve pondering the saliva of leeches, but now here’s your chance.
Hirudine is a clot or thrombin inhibitor that comes from the spit of same worms. In 2008, when Dr. Mary Han of Stanford injected it into mice with experimental autoimmune encephalomyelitis, a paralytic disease similar to MS, improvement in the animals’ motor weakness was noted.
Proteomics, a new age genome based analysis of proteins, has helped to identify proteins involved in many diseases including cancer and MS. This helped Dr. Han to determine that MS patients with MRI visualized chronic active plaques in the brain (i.e. those hotly inflamed and often related to ongoing signs and symptoms) were the plaques that showed several proteins involved in coagulation (clotting). What a fascinating new area of MS research and quite a different pathway of disease pathogenesis than that usually pursued in attempts to decipher the mystery of MS!
It remains to be seen whether plaque type determination and clot busters from leech saliva will substantially help MS patients, but proteomics based biomarker research would appear to represent an exciting new arena with many implications for the MS community.
Published On: January 06, 2009