Nerve fibre protection
Posted: Sat Nov 06, 2004 8:49 am
Dear all (couldn't keep away as I'd hoped),
Article from the UK MS Society's website. Key point is that the article claims that the research team have identified an effective therapy to protect nerve fibres. It says that the therapy appears to work well, and it should be safe and inexpensive. Annoyingly they are seeking funding to conduct a full clinical trial in MS patients (why can't they ever fast track the stuff - I'd be happy to sign a form and take the risk if it would potentially protect my nerve fibres from getting damaged). Anyone have any ideas what they might be considering? Looks like it is an existing drug. I'm sure that I've also seen that one of the major drugs companies is investing in neuro-protective drugs.
I assume the current thinking is to reduce attacks (which hopefully Antegren will do), help protect the nerve fibres that are attacked - by a neuro protector and, eventually, re-myelinate. Seems sensible to me (a layman) but I'm sure one of you (probably OddDuck) will come up with a very bright reason why this won't work.
OddDuck - what's your view on neuro protection?
Also, are there any plans to use stem cells to repair / replace damaged nerve fibres or will they only be used for creating myelin?
Bromley
Professor Kenneth Smith is Professor of Neurophysiology at Department of Neuroimmunology, King’s College, London.
Achievements in research:
I think it is best if other people describe this subject, as they have better perspective. However, in general I have tried to find out how demyelination changes the properties of nerve fibres, causing them to generate the symptoms of MS. Research from several laboratories has revealed that demyelination initially blocks conduction, causing symptoms such as visual problems, weakness and numbness, depending on which groups of nerve fibres are affected. However, nerve fibres can adapt to the demyelination and then conduction can be restored, leading to recovery from the symptoms.
Recovery does not always occur sufficiently, and then some residual symptoms can persist. Sometimes demyelinated nerve fibres can become hyperexcitable, and then they can generate tingling sensations, which are sometimes initiated by body movements. The demyelinated nerve fibres are sometimes repaired by remyelination, and when this happens normal function can be restored.
Together with my colleagues in the research community, I have tried to uncover why and how these changes in function occur. Most recently we have tried to understand why nerve fibres degenerate in MS. Once degeneration has occurred, function is likely to be permanently damaged because nerve fibres do not regrow in the brain and spinal cord. It is therefore very important to try to find ways to protect the nerve fibres from degeneration. We have found a potential reason why degeneration occurs, and we have identified an effective therapy to protect the nerve fibres. The therapy appears to work well, and it should be safe and inexpensive, and we are seeking funding to conduct a full clinical trial in MS patients.
Article from the UK MS Society's website. Key point is that the article claims that the research team have identified an effective therapy to protect nerve fibres. It says that the therapy appears to work well, and it should be safe and inexpensive. Annoyingly they are seeking funding to conduct a full clinical trial in MS patients (why can't they ever fast track the stuff - I'd be happy to sign a form and take the risk if it would potentially protect my nerve fibres from getting damaged). Anyone have any ideas what they might be considering? Looks like it is an existing drug. I'm sure that I've also seen that one of the major drugs companies is investing in neuro-protective drugs.
I assume the current thinking is to reduce attacks (which hopefully Antegren will do), help protect the nerve fibres that are attacked - by a neuro protector and, eventually, re-myelinate. Seems sensible to me (a layman) but I'm sure one of you (probably OddDuck) will come up with a very bright reason why this won't work.
OddDuck - what's your view on neuro protection?
Also, are there any plans to use stem cells to repair / replace damaged nerve fibres or will they only be used for creating myelin?
Bromley
Professor Kenneth Smith is Professor of Neurophysiology at Department of Neuroimmunology, King’s College, London.
Achievements in research:
I think it is best if other people describe this subject, as they have better perspective. However, in general I have tried to find out how demyelination changes the properties of nerve fibres, causing them to generate the symptoms of MS. Research from several laboratories has revealed that demyelination initially blocks conduction, causing symptoms such as visual problems, weakness and numbness, depending on which groups of nerve fibres are affected. However, nerve fibres can adapt to the demyelination and then conduction can be restored, leading to recovery from the symptoms.
Recovery does not always occur sufficiently, and then some residual symptoms can persist. Sometimes demyelinated nerve fibres can become hyperexcitable, and then they can generate tingling sensations, which are sometimes initiated by body movements. The demyelinated nerve fibres are sometimes repaired by remyelination, and when this happens normal function can be restored.
Together with my colleagues in the research community, I have tried to uncover why and how these changes in function occur. Most recently we have tried to understand why nerve fibres degenerate in MS. Once degeneration has occurred, function is likely to be permanently damaged because nerve fibres do not regrow in the brain and spinal cord. It is therefore very important to try to find ways to protect the nerve fibres from degeneration. We have found a potential reason why degeneration occurs, and we have identified an effective therapy to protect the nerve fibres. The therapy appears to work well, and it should be safe and inexpensive, and we are seeking funding to conduct a full clinical trial in MS patients.