A ground-breaking drug has been found to slow cognitive decline in people with Alzheimer’s - with experts hailing it a breakthrough that “can meaningfully change the course of the disease”.
The experimental drug - named Lecanemab - showed the promising effects in a trial that spanned 18 months and involved nearly 1,800 patients with early-stage Alzheimer’s.
Full data from the trial was published on Tuesday. The Alzheimer’s Association said the drug “can meaningfully change the course of the disease,” while calling on US regulators to approve the company’s application for accelerated approval.
Professor John Hardy, group leader at the UK Dementia Research Institute at UCL, said: “This trial is an important first step, and I truly believe it represents the beginning of the end.
“The first step is the hardest, and 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.”
Prof Bart De Strooper, director at the institute, added: “The overall conclusion is extremely positive. This trial proves that Alzheimer’s disease can be treated.”
Prof Nick Fox, director of the Dementia Research Centre, said: “I believe, it confirms a new era of disease modification for Alzheimer’s disease.
“An era that comes after more that 20 years of hard work on anti-amyloid immunotherapies – by many many people – and many disappointments along the way.”
Lecanemab is an antibody therapy designed to remove sticky deposits of a protein called amyloid beta - which builds up around brain cells in Alzheimer’s patients, affecting the ability of the cells to transmit messages to one another.
Companies Eisai and Biogen, which developed the drug, announced in September that the drug had reduced the rate of cognitive decline by a relatively modest 27 per cent.
The full trial data showed that some patients with a genetic risk of developing the mind-wasting disease did not benefit from Lecanemab, based on a clinical dementia scale named ‘CDR-SB’.
They did, however, show improvement under the trial’s secondary goals, including making progress in other measures of cognition and daily function.
Overall, Lecanemab patients benifitted by between 23 per cent and 37 per cent.
“I believe it’s an important benefit that will justify full approval. But of course, we want a bigger benefit,” said Dr Paul Aisen, director of the University of Southern California Alzheimer’s Therapeutic Research Institute and a co-author of the study published in the New England Journal of Medicine.
He said Lecanemab is likely to provide greater benefit if given earlier in the disease, “before you’ve accumulated enough irreversible damage to be causing symptoms”.
Experts believe the trial results prove a longstanding theory that removing amyloid beta from the brains of people with early Alzheimer’s can slow the disease’s progress.
They stressed more work is still needed to investigate Lecanemab’s side effects.
The US Food and Drug Administration is slated to decide by January 6 whether to approve Lecanemab under its “accelerated” review program, which requires proof that a drug can impact a biomarker associated with a disease, such as reduction of amyloid beta in the brain.
There are thought to be around 850,000 people living with dementia in the UK - representing one in every 14 people aged 65 and above. As of 2013, there were 42,324 people below 65 living with early-onset dementia.
Alzheimer’s is the most common type, thought to make up between 50 and 70 per cent of cases.
The Alzheimer’s Society estimates that if current trends continue without intervention, there will be an estimated one million people living with dementia in the UK by 2025.
