Alzheimer's disease is one of the most common in Britain. A new exhibition explains the illness and the progress towards a cure. Liz Hunt reports
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MOTHER: "I did think once that I had that disease ... Oh, you know. The one that makes you forget everything."

EDINA: "Alzheimer's?"

MOTHER: "The one that you get when you are old."

EDINA: (louder) "Alzheimer's."

MOTHER: "Yes, what is it called."

EDINA: (shouts) "Alzheimer's!"

MOTHER: (turning away) "Oh, I can't remember."

- 'Absolutely Fabulous'

Ten years ago it was an obscure illness with a peculiar name, a Cinderella candidate in the battle for charitable donations. Today Alzheimer's has all the trappings of the celebrity disease. Like heart conditions, cancer and stroke, it regularly makes the headlines, and consumes a lion's share of voluntary funds.

On Wednesday, a new exhibition on Alzheimer's opens at the Science Museum in London, possibly the first time a single disease has been accorded this status. Next month The Lancet medical journal will devote one of its prestigious conferences to the growing problem of the dementia cases, of which Alzheimer's accounts for two-thirds in Britain.

Alzheimer's disease, a degenerative brain disorder marked initially by memory loss, confusion and eventually by total disintegration of the intellect, owes its new-found status to the alarming statistics surrounding it. It is the single most common disease in Britain and the fourth major cause of death. Of the 650,000 cases of dementia in Britain, 390,000 are due to Alzheimer's, and doctors predict 120,000 new cases annually as the population ages.

Up to 500 people are diagnosed daily, according to the Alzheimer's Disease Society. On average, eight years elapses between diagnosis and death. At age 40-65, one person in 1,000 will develop Alzheimer's, rising to one in 50 at 65-70, one in 20 at 70-80, and one in five at age 80 and over. Nothing has highlighted so starkly the consequences of the demographic changes now facing the West.

"Most people will know of someone who has the disease," says Colin Uttley, director of programmes at the Science Museum. "It is a fear we have for ourselves and our parents."

Awareness of Alzheimer's is remarkably high, he says, but understanding of what it actually is, and an individual's chance of developing it - about one in 130 of those who visit the Exhibition will succumb - is poor. This is a situation that the Science Museum aims to rectify.

"Ten or 15 years ago senile dementia was a catch-all phrase to describe old people who were a bit forgetful dotty. Now it's Alzheimer's, but the disease is just one of a number of dementias," says Colin Uttley.

When the former US president Ronald Reagan announced he was a sufferer in November 1994, the Reagans were lauded for their decision to go public and acres of newsprint around the world were devoted to the condition. However, few appeared to question a fundamental flaw in the story. There wasn't then, and there isn't now, a single test to confirm Alzheimer's.

Diagnosis depends on exclusion of other causes of memory loss and confusion - it is only by looking at the brain after death that a definitive diagnosis can be made. Given that diagnosis before death is about 85 per cent accurate, this may seem pedantic - but it is precisely these kinds of misunderstandings the Science Museum wants to address.

A healthy brain is a central feature of the exhibition, which is part of the museum's Science Box series. Visitors can then view slices of diseased brain under a microscope. Normal brains have small clumps or plaques of a fatty protein, called beta amyloid. Alzheimer's patients' brains have thousands of plaques in the cerebral cortex or "thinking" centre. A protein called tau is an important part of the structure of normal nerve cells, but with Alzheimer's it forms tangles. The plaques and tangles destroy healthy cells.

Barely a week passes without some new Alzheimer's research "breakthrough" being announced; a handful are genuine, but the majority are tiny steps along the path towards an effective treatment or cure. The Science Museum exhibition aims to clarify the situation, focusing on the real milestones of research in the last 15 years. It will be opened this week by Dr Martin Rossor, a consultant neurologist at St Mary's Hospital, London, and the National Hospital for Neurology and Neurosurgery, and Britt Ekland, whose mother died of Alzheimer's.

"The progress has been remarkable," says Dr Rossor. "From a situation 20 years ago in which we thought Alzheimer's was an inevitable consequence of ageing, we have progressed to an excellent understanding of the disease at a molecular level."

Since 1991 scientists have found four genetic or inherited links for Alzheimer's. Three of these are for very rare abnormal genes which are responsible for the disease in people aged 60 and under. The fourth is a normal version of a gene and is more common. About one person in 50 carries it, and is ten times more likely to develop Alzheimer's as a result.

What this means for a treatment or even a cure is difficult to determine. There are already drugs in use, particularly in the US, which reduce some of the symptoms. Most work by boosting the amount of a chemical known as acetylcholine, which acts as a messenger between nerve cells. Tacrine is the best known of these. It is available in France and the US but not in the UK, where it was refused a licence by the Medicines Control Agency. British doctors believe it may give short-term relief to a small proportion of dementia patients in the early stages of the illness; there has been concern about side-effects including liver damage and nausea.

A substance called Nerve Growth Factor boosts brain cell connections and helps keep cells healthy, and scientists are looking into ways of delivering this to the brains of Alzheimer's patients in the hope that it might limit damage. But one of the most promising new lines of treatment relies on simple painkillers, the non-steroidal anti-inflammatory drugs (NSAIDS) taken by rheumatism sufferers. At the American Academy of Neurology meeting in San Francisco earlier this month, scientists said that people who took NSAIDS regularly were half as likely to develop Alzheimer's as non-users. Some of the changes in the brains of sufferers are inflammatory, and the American researchers hypothesise that the NSAIDS limit damage to brain cells.

The human element - the Alzheimer's victim's personality disintegration and the distress this causes - is another element of the exhibition, which will be concluded by a television documentary featuring writer Hunter Davies, whose mother died of the disease. "It is particularly sad for us," he said. "It includes home videos of my mother, and you see the disintegration. You live in hope of a breakthrough but until then, anything that can increase awareness has to be a help."

The Alzheimer's Disease Exhibition, 2 May-1 September, The Science Museum, Exhibition Road, London SW7 (0171 938 8123).