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Sunday, 25 November, 2001, 01:03 GMT
Gene link to MS severity
Multiple Sclerosis is a progressive, disabling condition
Scientists are hopeful that a way can be found to interrupt the destructive chain reaction that progressively damages multiple sclerosis patients.

A team at the University of California at San Francisco has found a gene that appears to play a key role in the sequence of physical changes that make up an MS attack.

It is possible that interfering with the activity of the gene - or the body chemical it produces - could both reduce the impact of a relapse, and perhaps cut the frequency of relapses.

The research is published in the journal Science, and involved work on brain tissue from both humans with MS, and mice with a similar condition.

Inflammation damage

In MS, a massive inflammation of nerve tissue destroys the material, myelin, which encloses and protects the nerves in the spinal cord.

As a result, communication between nerve cells can be disrupted, causing weakness, muscle spasms, or problems with vision.

Patients can suffer regular attacks, in between which they either recover, or which leave them progressively more and more disabled.


If there were medicines which affect osteopontin, it might provide an opportunity for interfering with this chain of events - perhaps even affect the course of this illness

Professor Alastair Compston, Cambridge University
The frequency and severity of these relapses is key to the speed at which a patient will deteriorate.

The research team are looking to unravel exactly what is happening in the body when an attack is underway - and which body chemicals are involved in causing this inflammation.

Looking at inflamed brain tissue from MS patients, they discovered an over-abundance of the gene which produces a chemical called osteopontin.

Genetically altered

Closer examination of the brains of mice with an MS-like condition revealed that osteopontin was present more prominently in inflamed areas during relapses - but not during the remission periods in between.

To test the other side of the equation, they created mice which were genetically-altered so they produced no osteopontin - and their MS-like illness was far less severe.

Not only was there less inflammation, but these mice did not have as many relapses.

This raises the possibility that, by removing osteopontin, and disrupting the "chain reaction" of the relapse in the middle, an as-yet unknown part of the reaction which governs the frequency of relapse further down the chain is also disrupted.

Doctors in theory could try to target osteopontin or its gene in an attempt to make this happen in a patient.

A British expert, Professor of Neurology Alastair Compston from Cambridge University, said it was a "very interesting study".

He told BBC News Online: "It is, potentially, a new target - if there were medicines which affect osteopontin, it might provide an opportunity for interfering with this chain of events - perhaps even affect the course of this illness."

See also:

21 Apr 01 | Health
MS sufferers 'let down' by NHS
06 Aug 01 | Health
'Beta interferon is my last hope'
07 Aug 01 | Health
Dying MS man fights to go home
07 Aug 01 | Health
Concern as MS drug 'rationed'
27 Nov 01 | Health
Cooling vest aids MS symptoms
17 Oct 01 | Health
MS reversed in lab
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