Alzhemier's might have link to brain infection Within two years, the world of Peter Dunlop has shrunk dramatically — the respected senior obstetrics and gynaecology consultant who once worked on high-risk births and performed complex operations almost every day is now a man who struggles to understand his daily post.
The married father-of-two switched from the role of doctor to patient with brutal speed when told, aged just 53, he had Alzheimer’s disease.
Overnight, his career was over.
‘Even if they had said I could carry on for a while, how could I have?’ he asks.
‘Obstetrics is one of the riskiest areas of medicine and if anything went wrong, even if it had been entirely unavoidable, I would have thought it was my fault. It would have left me suicidal.’
There were only nine months between a sudden panic-inducing mental blankness in the middle of a consultation, followed by a series of inexplicable black holes in his memory, and the confirmation of his worst fears.
‘It was awful,’ he says of that first lapse. ‘I suddenly had no idea what I was doing there, who the patient was or what I was meant to do.
'Luckily, the nurse knew something was wrong and took over the conversation.’
This episode was followed by similar incidents: where were his keys? Where was he going and why? How was he going to get there?
None of his medical colleagues at Macclesfield General Hospital in Cheshire noticed anything wrong, but once Peter saw his GP less than a month after the first memory blackout, his referral for expert assessment was swift.
Brain scans confirmed that his left hippocampus, one of the key areas responsible for memory and the first to be affected in Alzheimer’s, was shrinking.
Furthermore, the level of shrinkage suggested the mental deterioration had begun long before Peter experienced any symptoms.
The diagnosis was made on a Friday in the summer of 2009. By the following Tuesday, Peter had removed himself from the medical register.
‘I have seen so many women over the years who have experienced the most terrible bereavement and trauma,’ he says.
‘If terrible things happen even to the nicest people, then I have to accept there is no reason they shouldn’t happen to people like me.’
Alzheimer’s affects more than 800,000 Britons — by 2021, the number will be one million, a consequence of an ageing population and increasing rates of obesity, heart disease and diabetes, which increase risk.
However, Peter’s affliction came out of the blue — he was fit, healthy and had no family history of early onset Alzheimer’s.
As the number of cases without explanation such as Peter’s climbs steadily, scientists are engaged in a relentless quest to establish where the condition comes from and, most importantly, how to prevent it.
Alzheimer’s is characterised by the spread of faulty brain compounds called beta-amyloid and tau proteins — these lead to dead patches in the brain, destroying memory and thinking.
Where these proteins come from is unknown. However, evidence is emerging that might help develop effective treatments and ways to halt the progress of the debilitating condition.
Doctors have discovered the apparently random spread of the faulty proteins may, in fact, be a form of infection.
Recent research has shown that if a small number of abnormal protein cells are introduced directly into animal brains, they ‘infect’ cells around them, causing the proteins in these neighbouring cells tobecome abnormal.
Last month, Claudio Soto, professor of neurology at the University of Texas medical school, showed that if you infect mice brains with brain tissue from human Alzheimer’s patients, they, too, develop the disease.
In other words, once an abnormal protein arrives in the brain, it infects the proteins around it, with devastating consequences.
Research by Professor Soto and scientists in Germany has shown that if these abnormal proteins are introduced into other parts of the body, they can travel into the spinal fluid and up to the brain.
The discovery of this ‘seeding’ phenomenon has led to speculation that these so-called prions — a word that comes from combining protein and infection — may be spread by contaminated organ transplants, medical instruments during operations, or even dental instruments that are in direct contact with the rich blood supply to teeth and gums.
Also, like the prions that caused variant CJD dementia, the human form of mad cow disease, they might come from the food supply.
Doctors accept abnormal proteins are the cause of dementia, but the suggestion that the process might be caused by prions similar to those that cause CJD is new and may have dramatic implications.
‘In our experiments, we injected Alzheimer’s tissue directly into mice brains,’ says Professor Soto.
‘Obviously people do not normally have infectious agents injected into their brains, so we need to find out whether the disease can be transmitted by natural routes of exposure in humans.’
Mathias Jucker, a senior scientist at a research centre into neuro-degenerative diseases in Tubingen, Bavaria, one of the world’s centres of expertise in disease-causing proteins, has published a review of the evidence on infectious Alzheimer’s in the latest issue of the journal Annals Of Neurology.
He has speculated on whether human transplant surgery should be controlled to ensure donor organs are not taken from elderly, high-risk individuals who may be carrying abnormal proteins associated with Alzheimer’s.
He also thinks people who have undergone major surgery should be monitored to see if they are at greater risk of developing dementia, as a way of getting evidence that infectious proteins can be passed on.
‘These discoveries could mean we will at last find a way of preventing and treating this condition,’ he says.
‘But we have to bear in mind that if Alzheimer’s was really infectious, in the same way as measles or flu, we would know by now how it works.’
In other words, and this cannot be stressed enough, Alzheimer’s patients are not infectious. The disease cannot be passed on to other people ‘naturally’.
‘Studies have shown it is possible to transfer or “seed” these infectious proteins to laboratory animals under specific conditions, but we don’t know what that is telling us about the natural disease process,’ says Professor John Collinge, head of the department of neuro-degenerative disease at University College London and Britain’s leading expert on variant CJD.
‘Though you can inject the infection, I don’t think there is much evidence that it can be naturally transmitted.’
Professor Collinge was asked to organise a highly confidential gathering of leading international specialists in the field in New York last week. They discussed the implications of the growing body of knowledge on infectious dementia and how to target research most effectively.
Unravelling the precise nature of why some people are affected by Alzheimer’s while others are not is going to be a complex process — not least because exposure to surgical instruments is so common that proving a difference in rates of dementia between those who have had surgery and those who have not would be impossible.
Alzheimer's sufferer Peter Dunlop has undergone a variety of surgical procedures and dentistry over the years, dating back to when he had milk teeth removed in early childhood.
He is still sufficiently mentally alert to read medical journals and attend conferences on dementia, though he often immediately forgets what he has read.
However, he has understood that though it is clear that dementia is not infectious in the conventional sense, the evidence does show it can be passed on.
‘The notion of infection as a cause seems entirely plausible, but as these researchers are saying, it is difficult to work out how it gets there in the first place,’ he says.
‘Whether anything will come from this research in time to help the likes of me seems doubtful.
‘To be honest, once you have got Alzheimer’s, thinking about science and where it might all have come from does get increasingly difficult.
‘I will have to leave all that behind and concentrate on things that I can do and enjoy.’