Fortnightly treatment reverses brain changes in study tracking symptoms.
The treatment reverses pathological changes in the brain, removing a toxic protein that builds up in people with Alzheimer’s
Millions of Alzheimer’s patients have been given hope of a cure after a drug was proven to slow the disease for the first time.
Trial results confirmed that lecanemab — delivered as a fortnightly intravenous drip — slowed memory decline by 27 per cent over 18 months.
The new treatment reverses pathological changes in the brain, finding and removing a toxic protein called amyloid that builds up in people with Alzheimer’s disease. The “momentous and historic” study was presented last night at a packed conference of the world’s leading scientists and doctors in San Francisco.
Experts said that it was the biggest breakthrough in a generation, marking the “beginning of the end” of Alzheimer’s and offering “real optimism that dementia can be beaten and one day even cured”.
While lecanemab slows the disease, rather than halting it, it is the first drug to provide a treatment option. Scientists say that the discovery paves the way for a new era of treatments that will ultimately lead to a cure.
Alzheimer’s is the leading cause of dementia, which affects 900,000 people in the UK, and experts say that lecanemab could be available to patients by the end of next year.
The trial, published in the New England Journal of Medicine, involved 1,795 patients aged 50 to 90 who had had early Alzheimer’s disease diagnosed.
Half were given lecanemab and half given a placebo in the trial, which took place at 235 sites in North America, Europe and Asia. The severity of their dementia was scored using a clinical scale that took account of symptoms including forgetfulness, relationship problems, problem-solving skills and the ability to live independently.
The disease progressed in both groups over the 18-month study period, but worsened significantly less quickly in those taking lecanemab.
Participants also had blood tests and brain scans to look for levels of amyloid, a protein that forms clumps in the brain. The levels fell so dramatically in those taking lecanemab that some no longer met the threshold to have had a diagnosis of Alzheimer’s.
The peer-reviewed study was led by Professor Christopher van Dyck, director of the Alzheimer’s Disease Research Unit at Yale University. It confirmed a shareholder report issued two months ago by Biogen and Eisai, the US and Japanese pharmaceutical companies that developed lecanemab.
The study found that lecanemab was associated with side effects including headaches and microbleeds on the brain. Six patients treated with lecanemab suffered from strokes during the study, compared with two in the placebo group.
Rob Howard, professor of old age psychiatry at UCL, said: “This will encourage real optimism that dementia can be beaten and one day even cured.”
Dr Susan Kohlhaas, director of research at Alzheimer’s Research UK, said: “Although the benefits were small and came with significant side effects, it marks the arrival of a treatment that can slow the course of Alzheimer’s.”
Experts said the drug could be approved for NHS use next year, but that diagnostic tests to detect if people had amyloid in their brain were not widely available.
For the first time, we have proof that Alzheimer’s can be treated (Eleanor Hayward writes).
The trial results showing that lecanemab removes toxic proteins and slows the march of the disease build upon a breakthrough by British scientists three decades ago.
That 1989 research by Professor Sir John Hardy of UCL identified a protein called amyloid that clogs up the brains of people with Alzheimer’s.
This led to billions of pounds being poured into drugs and trials that target amyloid proteins. For the first time one has worked, and scientists know they are on the right path.
Lecanemab is an antibody — a type of protein produced by the immune system — that finds and removes amyloid. The discovery that it works will accelerate the development of other Alzheimer’s drugs, with 117 in trials including several others made from antibodies.
This could potentially lead to a range of medications adapted to the needs of individual dementia patients, with multiple treatments available — each targeting different aspects of the condition.
Responding to the lecanemab trial results, Hardy said: “I truly believe it represents the beginning of the end. The amyloid theory has been around for 30 years so this has been a long time coming.
We now know exactly what we need to do to develop effective drugs. It’s exciting to think that future work will build on this, and we will soon have life-changing treatments to tackle this disease.”
For this article in pdf, please click here: