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| TX: 21.11.05 - Dementia: Science PRESENTER: JOHN WAITE |
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| THE ATTACHED TRANSCRIPT WAS TYPED FROM A RECORDING AND NOT COPIED FROM AN ORIGINAL SCRIPT. BECAUSE OF THE RISK OF MISHEARING AND THE DIFFICULTY IN SOME CASES OF IDENTIFYING INDIVIDUAL SPEAKERS, THE BBC CANNOT VOUCH FOR ITS COMPLETE ACCURACY. WAITE Alzheimer's - the most common form of dementia - was first discovered almost exactly a hundred years ago. Since when many of the hundreds of other conditions, like Pick's Disease and vascular dementia have also been identified. But though we've increasingly mapped the scale of dementia coming up with effective treatments hasn't been so successful. Brian Anderton is professor of neuroscience and director of the new Medical Research Centre for Neurodegeneration of Research at the Institute of Psychiatry at King's College, London, and his team are looking into a number of new treatments for dementia, all of which start by understanding its causes. ANDERTON Dementia is a form of neurodegenerative disease and what that means is nerve cells degenerate, in fact they die. And the treatments we have right now they really only affect the symptoms. So it improves the day-to-day function for a while but it doesn't stop the disease sadly. And so eventually the disease overtakes them and they go downhill anyway. WAITE How do they work? ANDERTON By compensating for the loss of a chemical which is involved in communicating between one nerve cell and the next, it's a chemical called acetylcholine. And when it's released from one cell it hits molecules on the surface of the next cell, called receptors. Now you can't stimulate receptors continuously, it has to be for a very brief period - less than a second - and there's an enzyme on the surface of those cells that destroys the acetylcholine called acetylcholine esterase. Probably a cell that's sick just releases less acetylcholine when it needs to than it should do and the enzyme - acetylcholine esterase - destroys it very quickly before it can ever hit the receptors and get a response in the next cell. So the drugs we have at the moment inhibit that enzyme - acetylcholine esterase - so this smaller amount of acetylcholine that's released now doesn't get destroyed immediately but sufficient amounts of it can hit receptors and cause a stimulation. [Indistinct words] compensates for this lower amount of enzyme. But of course the cell eventually will die ... WAITE I was going to say - why does that effect wear off, why does it have to wear off, why couldn't the drug keep on doing that - because the cell basically is mortally wounded? ANDERTON Yeah, it is indeed and the cell is running out of steam and it might take weeks or even months for an individual cell to die, it's slowly running down and there will come a point when it can't even release enough acetylcholine even for the drugs to compensate and eventually the cell's dead. WAITE And these drugs can slow down the processes, you say, but only in some patients, so how far off are we from first of all discovering treatments that can slow down the progress for everybody? ANDERTON That is the $64,000 question. We don't know how long it's going to take but if there's, for example, a particular enzyme - not acetylcholine esterase - but another enzyme which is important in the development of the pathology and development of the cell death then if you can find drugs to hit that enzyme then maybe we'll stop the whole progress of the disease. WAITE But that's what you're talking about is it - stopping the progress, not curing the disease? ANDERTON If you could stop the progress then it could be that the brain will repair itself, particularly if you could treat people in the early stages. So neuropathologists have known for a long time that there's evidence of what we call neuronal sprouting in the Alzheimer brain - that's an attempt for nerve cells to grow new connections. We all know that many people have strokes, although they may never recover completely they do over a period of time recover quite a lot of function, so why not in Alzheimer's Disease. If you could stop the cell death then maybe we could recover a reasonable amount of function. WAITE And one thing that's become clear to me during this month on dementia is how many people are affected, those numbers seem to be increasing but how relatively little - well in fact almost puny is the amount spent on research. ANDERTON You're quite right. If you look at the total cost it's estimated to be anywhere between £7 and 14 billion per annum in this country. Whereas the cost of cancer, which of course is an important disease, is much less than that. When you compare the amount of money spent on research much more money is spent on cancer research than it is on Alzheimer's Disease and we do just need to invest more in research to find cures much faster. WAITE Before we leave the subject of research though there has been, again as I understand it, recent excitement about a vaccine. Can you explain what that's about? ANDERTON Many people have an injection for flu and what one's injected with is disabled flu virus. And that induces an immune response, which means we make antibodies to that flu virus. So then a few weeks later when we actually get an infection from flu from somebody else who's got the disease our antibodies immediately remove the offending flu virus and we never actually develop any symptoms. Now in the case of Alzheimer's Disease one of the changes in the brain is a deposit of a small protein called amyloid and we think that's very important in the disease. So patients are being immunised with the amyloid protein, they make antibodies to the amyloid protein and we have good reason to believe that those antibodies then actually remove the already deposited amyloid in the brain. And unfortunately those sorts of responses often induce an inflammation, which in the case of many diseases we can put up with, we can tolerate, but we can't tolerate inflammation in the brain. And so when some of the patients who were on this vaccine developed inflammation the trial was then stopped and what scientists are trying to do in industry and academia is to try and get around the inflammation problem, so that if we could avoid the inflammation then maybe an amyloid vaccine would really be of great benefit. WAITE And is there any hope with stem cells - could they help in this area? ANDERTON Well stem cells are cells that can develop into any other sort of cell and there are different degrees of differentiation, going down the road from a cell that can develop into a liver cell or a nerve cell, to stem cells that are particularly predestined to become nerve cells and they do exist in the brain already. And their role would be that it could replace or repair the damage and replace the lost nerve cells in the brain. And it might well be that stem cells will be used first to treat diseases like Parkinson's Disease or Huntingdon's Disease because in those diseases there are very specific areas and relatively small areas of the brain that degenerate. Unfortunately in Alzheimer's Disease it's large areas of the cerebral cortex, the surface of the brain, that degenerate. And so the repair problem is much, much greater, it's not simply replacing a little bit in the motor in your car but it's replacing the whole engine. So I think although it would be foolish to say stem cells will never be used to treat Alzheimer's Disease I think we're really a long way off before we can actually hope that is going to be used. WAITE So, finally, I mean realistically is there light at the end of the tunnel or I mean have you any hope you can extend to people? ANDERTON Yes, of course there's light at the end of the tunnel. But how long is the tunnel? There are already drugs developed by the pharmaceutical industry that are in clinical trials but it's still to early to know whether a. they're safe and b. whether they will actually be effective. And so I think one should be optimistic but I think it's just simply rash to say it'll be in two years, five years, ten years - we just can't put a timescale on it. WAITE Professor Brian Anderton. And tomorrow we'll be examining some home grown remedies for tackling dementia, asking whether eating fish or doing the crossword everyday - as many people say - can really help slow down the progress of the condition or as some say prevent it altogether. And if you want, of course, to hear any of our items on dementia again you can find them on our website at bbc.co.uk/radio4/youandyours. Back to the You and Yours homepage The BBC is not responsible for external websites |
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