Bob,
Here is an article from the UK MS Society's MS Frontiers conference in 2005 about the trial which MUU is on. It's pretty clear from this and the other presentations that MS is a complex disease involving many mechanisms. Harry Z does these researchers a disservice by suggesting that they are stuck in an 'MS is an auto-immune disease' rut. They've moved well beyond this and are trying to unpick the various strands of this disease. It is highly likely that different therapies will be required to tackle this disease - stopping inflammation / relapses; protecting nerve fibres and cells; and repairing those nerve fibres and cells which have been damaged.
As for 'cancer drugs', the jury is still out but they have shown some promise. Those in the RR phases have seen good results from Campath and Rituxan may well show promise (we await the results of the RR and PP MS trials). The work undertaken by Dr Freedman in Canada (Bone Marrow Transplantation) which uses high powered cancer drugs also looks promising. Cancer drugs can look scary, but so did Richard Pryor in his final years! In Harry's world no-one should take the CRABs because they are useless; Tysabri is expensive and doesn't do much; anti-cancer drugs just shake-up the immune system. Lucky for him that he doesn't have to make such a decision.
As MUU says, it's up to individuals to decide what is in their comfort zone in terms of treatment / trials. I'm convinced that the experts are unpicking this disease and are making progress - it's taken a long time because it is complex and new technology will provide more insights.
Ian
Quote:
MS Frontiers 2005 - Trials of neuroprotection in MS: present and future
Dr Raj Kapoor from The National Hospital for Neurology and Neurosurgery, London, focused on clinical trials of neuroprotection in MS.
Until recently, it was thought that disability in MS was caused mainly by the gradual loss of the fatty insulating layer of myelin which surrounds nerve fibres (axons), and which allows them to conduct electrical signals. However, we now know that most of the permanent disability in MS occurs because the axons themselves degenerate.
Experience suggests that the current strategy of modifying the immune system may not be able by itself to prevent this axonal degeneration and consequent disability, and that we will need to develop a second strategy, called neuroprotection, to achieve this goal. In order to do so, we will need to identify and to inhibit the mechanisms by which axons are damaged.
Research work has already identified several such mechanisms. For example, our group has shown that axons may be flooded with toxic levels of sodium from the surrounding tissue fluid as a result of inflammation in MS, and that the resulting damage can be prevented by drugs which reduce the entry of sodium. As a result, we have been awarded a grant by the Multiple Sclerosis Society to carry out a clinical trial to test the neuroprotective effects of one of these sodium channel blocking drug, lamotrigine, in people with the secondary progressive form of MS. We will randomize people in the trial to receive treatment either with lamotrigine or with an identical placebo (i.e. dummy) tablet for two years.
We will be able to compare the effect, of lamotrigine with the placebo, on the gradual shrinkage of the brain caused by axonal degeneration. This will be done by carrying out MRI scans at regular intervals. We will also measure the actual levels of disability in the two groups to assess the extent to which the treatment slows down its progression. This is likely to be the first of a number of trials which seek to block axonal degeneration by inhibiting the mechanisms by which the axons are damaged, and which offer new hope of treatments which can prevent people with MS from becoming disabled.
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