Slow protein clearance 'clue to Alzheimer's'
- 10 December 2010
- From the section Health
Scientists suggest people with Alzheimer's disease clear a damaging protein from their brains more slowly than those who are healthy.
It was already known that the beta-amyloid protein built up in the brains of people with the condition.
But the US study in Science suggests it is the poor clearance of the protein, not the build-up, that is the problem.
UK experts said the study of 24 people was small, but exciting, and could help understanding of the disease.
The ageing population means that dementia, including Alzheimer's, is currently seen as one of the main health challenges in the UK.
Numbers affected are set to soar - figures suggest that more than a million people will have developed the disease before 2025.
Using a spinal needle to collect the fluid, the team of neurologists from the University of Medicine in St Louis measured the amount of beta-amyloid in the brain fluid of 12 patients with late-onset Alzheimer's, and 12 patients who did not have the disease.
The levels were then sampled every hour for 36 hours.
It was found that the clearance of beta-amyloid in people with Alzheimer's was 30% slower than those without the disease.
They suggested beta-amyloid clearance rates could eventually be measured, perhaps via a blood test, in order to detect Alzheimer's before the symptoms appear.
And they added that the results meant scientists could now look at how beta-amyloid is moved out the brain. This in turn could help scientists develop drugs to target that process.
The study of was welcomed by the Alzheimer's Society.
Dr Clive Ballard, director of research, said: "This exciting study gives us an insight into the building blocks of Alzheimer's disease.
"We now need further research to find out why the system is not working properly and whether amyloid is toxic in higher concentrations.
"The burning question is whether this process starts before the onset of symptoms as this could be vital to the development of new treatments."
However Dr Simon Ridley, head of research at the Alzheimer's Research Trust, was more cautious. He commented: "As the researchers themselves point out, this was a small study, and it is not yet clear whether increased amyloid is a cause of Alzheimer's or a symptom of it.
"If we are to find the answers to these elusive questions and find an effective treatment for dementia, we must invest in more research."