Lesion load / auto-immune theory
Posted: Mon Nov 01, 2004 1:43 pm
Dear all,
Many MS treatments refer to the effectiveness they have on reducing the 'lesion load'. In the case of Antegren, the speculation is that the effect might be much higher than current treatments. What does this term mean? Having less lesions (I assume) is a good thing and would result in less damage to the myelin and the underlying nerve cells. I assume that having less lesions would also allow the body to deal more effectively with the remaining lesions (now fewer in number). This is my layman's (no science / medical background) interpretation - am I right to assume this?
Most research papers I have read seem to start from the basis that ms is an auto-immune disease. The theory seems to be that it is rogue immune cells which attack the myelin which leads to nerve damage etc. Most of the drug companies seem to buy into this theory and invest in new treatments accordingly. When you look at the research projects underway, the majority appear to focus on immunology. But many posts on this site, have suggested that ms may not be an auto-immune disease -although it may be part of the disease. Who out there (i.e. in the research world) is looking at other possibilities? I assume that the myelin might start to break down for other reasons (for example, death of the cells underlying it). The immune system may be just doing what it thinks is a repair job (which scars usually are), but this is being interpreted as the cause of the disease. Has any work been done to disprove this theory?
On another issue, I have read on a number of web sites that those who experience sensory symptoms at the first attack (rather than motor symptoms) have a better chance of a milder course of ms. Why should this be so? Surely, the attacks are random and future attacks could well effect motor functions etc?
Again, apologies for all the questions but so many of you have such a wide knowledge of what's going on in relation to this disease.
Thanks
Bromley
Many MS treatments refer to the effectiveness they have on reducing the 'lesion load'. In the case of Antegren, the speculation is that the effect might be much higher than current treatments. What does this term mean? Having less lesions (I assume) is a good thing and would result in less damage to the myelin and the underlying nerve cells. I assume that having less lesions would also allow the body to deal more effectively with the remaining lesions (now fewer in number). This is my layman's (no science / medical background) interpretation - am I right to assume this?
Most research papers I have read seem to start from the basis that ms is an auto-immune disease. The theory seems to be that it is rogue immune cells which attack the myelin which leads to nerve damage etc. Most of the drug companies seem to buy into this theory and invest in new treatments accordingly. When you look at the research projects underway, the majority appear to focus on immunology. But many posts on this site, have suggested that ms may not be an auto-immune disease -although it may be part of the disease. Who out there (i.e. in the research world) is looking at other possibilities? I assume that the myelin might start to break down for other reasons (for example, death of the cells underlying it). The immune system may be just doing what it thinks is a repair job (which scars usually are), but this is being interpreted as the cause of the disease. Has any work been done to disprove this theory?
On another issue, I have read on a number of web sites that those who experience sensory symptoms at the first attack (rather than motor symptoms) have a better chance of a milder course of ms. Why should this be so? Surely, the attacks are random and future attacks could well effect motor functions etc?
Again, apologies for all the questions but so many of you have such a wide knowledge of what's going on in relation to this disease.
Thanks
Bromley