- Cluster of genes identified which makes people vulnerable to the disease
- These people are less able to get rid of proteins that form clumps in brain
- Finding could help scientists develop a way of treating dementia
Colin Fernandez, Science Correspondent For The Daily Mail
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A cluster of genes has been identified in healthy brains that could help develop preventative treatments for Alzheimer’s disease.
People with the gene ‘signature’ – a sequence of between 50 and 60 specific genes – are vulnerable to the spread of the illness which causes dementia.
They are vulnerable because they are less able to get rid of the rogue proteins that cause plaques and tangles in the brain.
A cluster of genes has been identified in healthy brains that makes certain people more vulnerable to Alzheimer’s disease. Pictured, scans of sufferers’ brains (file photo)
University of Cambridge academics say the findings could be used to develop treatments for individuals well before symptoms appear.
At present, a genetic cause for Alzheimer’s has been found for only around 1 in 20 cases, and the researchers hope the breakthrough will cast light on the other 19 out of 20 cases that cannot be predicted.
The results, published in the journal Science Advances, looked at 500 healthy brains of people who died between the ages of 24 and 57.
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They found that brains with the signature are significantly weaker in the areas where Alzheimer’s disease spreads than brains that do not have the signature.
The researchers believe that healthy young people with this specific gene signature may be more likely to develop Alzheimer’s in later life.
ARE SKINNY PEOPLE MORE LIKELY TO GET ALZHEIMER’S? BEING UNDERWEIGHT ‘DRIVES UP RISK OF DEVELOPING DISEASE’
Many strive to stay trim as they age to avoid the crippling effects of diabetes and hypertension.
But a study warns too much weight loss could drive up our risk of developing Alzheimer’s disease.
Experts at Massachusetts General Hospital have found a link between low body-mass index and a build-up of amyloid plaques in the brain, which fuel the devastating brain disorder.
The findings have been hailed as a necessary warning for people to eat well and exercise, rather than simply dieting to stay slim.
In fact, the study’s author even speculates that people should be advised to put on weight as they age.
They would also most benefit from preventative treatments if and when they are developed for human use.
Earlier this year, the same researchers proposed that ‘neurostatins’ could be taken by healthy individuals to slow or stop the progression of Alzheimer’s, in a similar way to how statins are taken to prevent heart disease.
The new research could help identify who would benefit most from taking these in early life.
Although a neurostatin for human use is still quite some time away, a shorter-term benefit of these results may be to breed genetically modified mice or other animals that repeat the full pathology of Alzheimer’s, which is the most common way for scientists to understand this or any disease to develop new treatments.
Alzheimer’s disease is currently incurable.
Its molecular origins are also unknown, and it is hoped the gene signature research will help explore why certain parts of the brain are more vulnerable than others.
Professor Michele Vendrusculo of the Centre for Misfolding Diseases at Cambridge’s Department of Chemistry, one of the paper’s authors, said: ‘To answer this question, what we’ve tried to do is to predict disease progression starting from healthy brains.
‘If we can predict where and when neuronal damage will occur, then we will understand why certain brain tissues are vulnerable, and get a glimpse at the molecular origins of Alzheimer’s disease.’
Rosie Freer, a PhD student in the Department of Chemistry and the study’s lead author, said: ‘I hope that these results will help drug discovery efforts – that by illuminating the origins of disease vulnerability, there will be clearer targets for those working to cure Alzheimer’s disease’.
The findings could be used to develop treatments for individuals well before symptoms appear, researchers said (file photo)
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