Dementia: I have a 50:50 chance. But I try not to worry
Peter Popham meets the remarkable family from Nottingham who changed the way scientists thought about Alzheimer’s - and offered hope to millions
Suddenly, Alzheimer’s Disease is the new frontier. Like cancer and HIV/Aids when they were thrust into the public consciousness, it presents a massive research challenge. At present there is no treatment for it: some drugs slow its progress, but there are no cures and no way of preventing it. Once the symptoms appear, it is like a cancer that has already metastasised, and by then it is too late – the brain has already suffered irreversible damage. So how can victims be identified before symptoms appear?
Meet Carol Jennings.
In the late 1980s, a team of neurologists at St Mary’s Hospital in west London was hunting the gene which caused familial Alzheimer’s when a letter arrived from a teacher in Nottingham. The decision of Carol Jennings to contact them about her family’s tragic history was to momentously advance our understanding of how and why Alzheimer’s strikes.
It didn’t stop there. As the years went by, word arrived that more members of her father’s family were behaving similarly as they approached 60. “Gradually it was going through the family,” she says. “It seemed like each year another one would have developed it. They would ask you something and five minutes later they were asking you the same question.
“I was thinking, what’s going on here? There’s this one, and this one and this one – and I thought, somebody ought to know about this.”
So in 1987 she decided to act. Her GP had told her about the team at St Mary’s Hospital that was researching the causes of Alzheimer’s. Already they had started canvassing for families with the disease through the networks of the Alzheimer’s Society. And one day she took out a sheet of Basildon Bond and wrote down her family tree, indicating those who had the disease and those who didn’t.
Rossor comments now: “Carol was very perceptive in seeing the importance of her relatives for research.” As this variant of the disease was inherited, with every child having a 50:50 chance of succumbing to it, by screening all family members the researchers could log the genetic differences between those with the disease and those without it. The team was able to establish beyond doubt that the family’s disease was caused by a mutated gene on chromosome 21 – “the same gene,” Rossor point out, “that codes for the amyloid protein that was observed by Alzheimer.” Those with the gene got the disease; those without it did not. There was no room for doubt.
Will it produce a cure? Rossor is cautious. “There aren’t many cures in medicine,” he says, “but amelioration can be dramatic. Recovery of the brain’s deficit in patients who already have symptoms may not happen, but by getting in at a very early stage of the disease we may be able to delay its onset and progression.”
Meanwhile, Carol and her family must deal with the frightening fact that half of them will develop the disease. Carol is now 58, the same age as her father when he first started making mistakes in his accounts, but she is not tempted by the idea of learning whether she too carries the mutated gene on chromosome 21.
To have the test, you’ve got to actually go to them and say, I want to know,” she points out. “And I never did want to know. Having the test has always been an option: I could find out now. But I think I would just collapse in a heap if I thought, ‘This was it’.”