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YOU would have to twist a doctor's arm a lot before he would admit that there could possibly be any health benefits from smoking. But for the past decade there has been nagging evidence that smokers suffer less than other people from Alzheimer's disease, and that this is not merely because they tend to die before the symptoms would otherwise appear. Now, a piece of research published in the Proceedings of the National Academy of Sciences, by Tobin Dickerson and Kim Janda, of the Scripps Research Institute in La Jolla, California, provides a possible explanation.

What causes Alzheimer's disease is not yet known for sure. But what is indisputable is that one of its main anatomical characteristics is the appearance of so-called amyloid plaques in the brain. These are huge gatherings of small protein fragments called amyloid beta peptides. Many researchers believe it is the formation of these plaques which causes the destruction of nerve cells that, in turn, produces the behavioural symptoms of the disease. If this is true, stopping the plaques from forming should stop the disease from progressing.

Health Tobacco The Proceedings of the National Academy of Sciences publishes an abstract of the research paper (full version available to subscribers). America's National Mental Health association has a fact sheet on Alzheimer's disease. The American Health Assistance Foundation offers more information on amyloid plaques.

Ever since the first suggestion that smoking might be protective, people have looked at tobacco to see if something in it inhibits plaque formation. Most have concentrated their attention on nicotine, since that drug is active in the brain, but with no great success. What Dr Dickerson and Dr Janda did was to look not at nicotine itself, but at nornicotine, one of the molecules that nicotine is turned into by the body, and particularly by the brain.

Dr Dickerson and Dr Janda have found by experiment that nornicotine is good at participating in a reaction called glycation, in which it reacts with glucose to form a molecule that goes on to react with a protein. They also observed that one specific place on the amyloid beta peptide should be especially susceptible to glycation. The shape of the resulting molecule means that glycating this site would, in turn, make it hard for the peptides to link up to form plaques.

And so it has proved. When nornicotine, glucose and peptide were incubated together, the result was a modified peptide that had little tendency to agglomerate. The mystery of the protective effect of smoking may now have been solved, although it remains to be seen whether a similar effect can be shown in brains.

None of this, everybody is keen to explain, should in any way be regarded as endorsing smoking. And it would surely be foolish to take the habit up early in life merely on the off-chance that it might ward off dementia in old age. But smoking takes years to impose its toll, so it is at least worth speculating whether the odd puff in late middle age might actually do more good than harm.