Yes Lynda Carol, I quite agree, it would definitely be a good thing to find out what kind of disease we have. We know what it’s called but not what it is only that we have it. Fine fix IMO.
About that “sick micro environment”, here’s an interesting (IMO) abstract on the matter. It seems to suggest that the neurodegeneration seemingly evident in MS may not even be totally dependent on the inflammatory process. Modulating Processes within the CNS is Central to Therapeutic Control of MS
neurodegeneration appears to be at least partially independent from neuroinflammation….. It is likely that immunomodulatory treatments acting purely in the periphery will provide only indirect and not direct neuroprotection…
The pathogenic process in the central nervous system itself should be the major focus in multiple sclerosis therapy in order to protect against demyelination and axonal loss and to promote remyelination and regeneration directly in the target tissue, independently of peripheral immune status. In conclusion, selective treatment strategies aimed at preventing axonal injury within the central nervous system are required to complement existing, peripherally acting treatments targeting the immune system.
For my 2 cents, I still like the idea that one factor in the “sick micro environment” might be glutamate toxicity. The recent front page article suggests damage to the oligodendrocytes happens first and the inflammation follows. This abstract
seems to suggest that oligodendrocytes could be susceptible to glutamate toxicity since they have those “NMDA receptors”.
Oligodendrocytes are known to express (Ca2+)-permeable glutamate receptors and to have low resistance to oxidative stress, two factors that make them potentially susceptible to injury…….Previous studies had failed to detect NMDA receptor mRNA or current in oligodendrocytes but three new papers demonstrate NMDA receptor expression in oligodendrocytes.
I’ve no scientific or medical background whatsoever, but I’ve latched onto these NMDA receptors and the notion of “glutamate toxicity” since the little bit I think I might understand seems to support the notion that theoretically it could account for damage to the myelin, axons and neurons in people with MS and be part of a “sick micro-environment”.
The good news is there are several things already on the market that might help minimize it, i.e., the memantine I posted some info about recently, several hormones, and minocycline. I think glutamate toxicity is also part of the thinking about how ldn may work. So, even if MS is not “auto-immune”, and I personally don’t think it is, I’m still optimistic that we could be a lot closer to more effective treatment than we think.
Even if we don’t know what kind of disease it is
I do think the researchers may have made some progress in understanding the molecular injury cascade. I'm sure hoping that's the case.