SCIENTISTS have discovered a gene that could slash your risk of Alzheimer’s by up to 70 per cent.
The genetic variant allows disease-causing proteins to pass out of the brain instead of clumping up, US researchers found.
The discovery could lead to new treatments that help reduce people’s chances of developing dementia, they said.
Dr Caghan Kizil, of Columbia University, said: “Our findings suggest that some of these changes occur in the brain’s vasculature.
“We may be able to develop new types of therapies that mimic the gene’s protective effect to prevent or treat the disease.”
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Around 944,000 Brits are currently living with dementia and experts predict the numbers will exceed one million by the end of the decade.
Alzheimer’s disease is the most common form of the condition, and is thought to be caused by build-ups of proteins in the brain, including tau and amyloid.
There is currently no cure for the disease, although promising drugs to slow down its progress are currently in trials.
The study, published in Acta Neuropathologica, looked at the genes of people who are more at risk of Alzheimer’s but haven’t developed symptoms to see what was protecting them.
Researchers looked at data from 11,000 people, including those who had inherited the e4 form of the APOE gene, which significantly increases the risk of developing the disease.
Dr Badri Vardajan, of Columbia University, said: “These resilient people can tell us a lot about the disease and what genetic and non-genetic factors might provide protection.
“We hypothesised that these resilient people may have genetic variants that protect them from APOEe4.”
They found a genetic variant that affects fibronectin — a substance in the blood-brain barrier, which controls what can get in and out of the organ.
The variant helps prevent too much fibronectin building up, allowing amyloid proteins to escape and reducing their likelihood of causing Alzheimer’s.
Dr Kizil said: “Alzheimer’s disease may get started with amyloid deposits in the brain, but the disease manifestations are the result of changes that happen after the deposits appear.
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“We may need to start clearing amyloid much earlier and we think that can be done through the bloodstream.
“That's why we are excited about the discovery of this variant in fibronectin, which may be a good target for drug development.”
