New treatments for Alzheimer’s that significantly slow down its progression could become available through the NHS in the next few years, experts said at a conference last week.
The drugs, which are in late-stage trials, work differently to the two antibody treatments that have been rejected for NHS use – and should be more potent.
“The science now gives us real reason for hope,” said Professor Catherine Mummery, a neurologist at University College London. “Within a few years, dementia care could look really different.”
Alzheimer’s, which causes memory loss and confusion, is currently treated only with drugs that slightly alleviate symptoms – but don’t stop the root cause of the illness.
The disease arises from a build-up of toxic proteins that kill brain tissue. One called amyloid, which has long been thought chiefly responsible, forms large plaques between brain cells. Another, called tau, builds up inside cells.
So far, most experimental therapies have targeted amyloid. Two drugs that clear amyloid from the brain, called lecanemab and donanemab, have been legally approved for use in the UK, but they cannot currently be given through the NHS.
That’s because they lead to only a small reduction in how much memory loss progresses over time – too small to be noticed by most people.
Their benefits don’t outweigh their costs, was the verdict from Nice, the cost-effectiveness body for the NHS in England, whose decisions also tend to be followed in Wales and Northern Ireland.
That ban is currently under review. But the two drugs have also met resistance because of their side effects, causing brain swelling or bleeding in up to a quarter of patients, which means people need regular hospital checks.
Second-generation antibodies
But soon there may be better options: 36 experimental treatments are in final-stage trials, with two in particular raising hopes of clinicians, said Professor Mummery at the Alzheimer’s Society annual conference this week.
One is a new amyloid-targeting drug that looks better for both effectiveness and safety. Called trontinemab, it works in a similar way to the first two, in that it’s an antibody that binds to amyloid, causing the protein to be cleared by the immune system.
The difference is trontinemab can pass more easily from blood into brain tissue, by exploiting the fact that cells of blood vessel walls have a molecular “shuttle” that transports iron from blood into the brain.
In trontinemab, the amyloid antibody is joined to a protein that locks onto that iron shuttle, leading to transport of the antibody into the brain.
According to results from a small trial, this has two net effects. It causes faster clearance of amyloid. And fewer people had the side effects typically seen with amyloid antibodies, of brain swelling and bleeding – less than 3 per cent.
With the first two amyloid drugs, the swelling and bleeding happens because amyloid builds up not just inside the brain but also in walls of blood vessels. When that amyloid is cleared by the immune system, blood vessels get damaged.
But with trontinemab, a relatively lower dose can be given, and the iron shuttle quickly takes it from blood to the brain, leaving blood vessels relatively unscathed. “The brain shuttle is way faster and has less side effects,” said Professor Ramin Nilforooshan, a psychiatrist at the University of Surrey.
Now, the treatment is being tested in larger, final-stage trials, which are due to complete in two years. If approved by Nice, trontinemab could be available through the NHS by 2029.
Brand new target
Another potential new treatment called diranersen highlighted at the conference targets the second toxic protein in Alzheimer’s, called tau.
Levels of tau in the brain seem to correlate more closely with a patient’s memory loss and it is the main focus for Alzheimer’s blood tests currently in development.
So far there has been no way reduce tau, because it is inside brain cells. But diranersen uses a new approach called “gene silencing” which turns off production of tau inside cells.
Results of a 416-person trial announced in May showed that it slowed cognitive decline by about 25 per cent.
Although this figure missed the manufacturer Biogen’s target, the firm has decided it is promising enough to progress to the final-stage trials needed for approval. “It is exciting because it’s a different method,” said Professor Mummery.
Professor Rob Howard, an old age psychiatrist at University College London, said we can’t know whether the new medicines will work until the larger trials produce results. “I think it’s premature to be getting excited about drugs until we’ve got the results of the trials that will actually tell us whether they work or not,” he said.
The trial of diranersen is likely to take longer to produce results, perhaps not until 2030, so it could be five years before it reaches the NHS, assuming all goes well.
However, by then it is possible that patients could be offered treatments against both kinds of toxic proteins to give the maximum chance of halting their decline. “We should give an anti-amyloid therapy very early on, anti-tau therapy very early on,” said Professor Mummery.
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