I agree with you completely Rita
There are two real obstacles in our way.
Firstly our understanding of the brain and it's associated diseases is woefully incomplete. New discoveries happen all the time but they only advance our knowledge by tiny increments. Evolution has taken millions of years to perfect this complex organism we call home, I suspect it will be many, many years before science fully understands it's intricacies.
Secondly drug discovery is an extremely expensive business. It requires the resources of the pharma companies just to get a drug off the drawing board, let alone into clinical trial. Once a drug is approved for use it is far more profitable to see whether it will work for other conditions than it is to try and discover new ones.
Of the available drugs, Copaxone is the only one that I am aware of that was specifically designed for MS. The interferons were originally aimed at HIV, All of the chemo drugs came from either leukemia or organ transplant. [Tysabri was designed for MS but is currently not available]
We are not only fighting MS but also economics.
Having said that, the influence of the pharma companies is not total. I will talk about the Campath trials because I have knowledge in that area, not for any wish to promote the treatment. The UK arm of the Campath trial is run by Cambridge university. To the best of my knowledge none of the scientists running the trial have any financial interest in the success of the trials. The drug itself is provided free by Schering/Genzyme but administration takes place at the wellcome clinical trust facility at Addenbrookes, a non-aligned research facility. Personally I have never seen any bias in favour of the treatment.
Success in fighting MS will come from the co-operation between research and commercial interests. There is no other way.
As a footnote I was at Addenbrookes today for one of my regular check-ups. One question I asked was if they had followed the SPMS patients who continued to progress long enough to see whether they stabilised over time. My reasoning being that if there was sufficient damage axons would continue to degenerate in the absence of active disease. Once the pre-conditioned degeneration had worked it's way out the patients would then stabilise. The answer surprised me somewhat in the fact that they hadn't followed the patients with that in mind. When I asked why, the answer was that as there was such a small number of patients and as MS is so variable no data would reach statistical significance either way.
I must admit that did strike me as going for the easy target first but what do I know?
Do not go gentle into that good night. Rage, rage against the dying of the light.