Millions of people could one day be given a “neurostatin” drug to guard against the early development of Alzheimer’s, new research suggests.
One drug, an anti-cancer agent called bexarotene, has already been shown to prevent early brain changes linked to the disease in laboratory tests.
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Scientists are in the process of identifying others that might be more effective.
The drugs have been dubbed “neurostatins” because they could be used in the same way statins are to reduce cholesterol and curb the risk of heart disease.
In this case they would be taken as a preventative strategy to keep out the seeds of Alzheimer’s, accumulating clumps of toxic protein in the brain.
Professor Michele Vendruscolo, from Cambridge University, who is leading the research, said: “This in terms of an approach for Alzheimer’s disease would be the equivalent of what statins do for heart conditions. So you would take them well in advance of developing the condition to reduce your risk.
“The dream would be to find a compound which is cheap and safe and therefore can be given early to everybody.”
He explained that Alzheimer’s and other neurodegenerative diseases occur in old age when natural defences that prevent the formation of protein aggregates in the brain, and help to clear them away, start to fail.
“Our idea is that we should supplement these natural defences by this chemical means,” he said.
Bexarotene was the first of about a dozen potential neurostatins identified by the scientists, whose research is reported in the journal Science Advances.
Dr Rosa Sancho, chief scientist at Alzheimer’s Research UK, said: “We know that the accumulation of amyloid is a hallmark feature of Alzheimer’s and that drugs to halt this build-up could help protect nerve cells from damage and death.
“A recent clinical trial of bexarotene in people with Alzheimer’s was not successful, but this new work in worms suggests the drug may need to be given very early in the disease.
“We will now need to see whether this new preventative approach could halt the earliest biological events in Alzheimer’s and keep damage at bay in further animal and human studies.”