Alzheimer’s support groups have hailed as “historic” the results of a new trial on a drug that aims to slow the progress of the most common form of dementia.
Clinical trials of the drug lecanemab showed that it slowed the decline of brain function by around 25 per cent throughout an 18-months treatment program.
The results, published this week in the New England Journal of Medicine, have been described by Dr Susan Kohlhaas, director of research at Alzheimer’s Research UK, as a “truly a historic moment for dementia research”.
Welcoming the release of the results, Dr Kohlhaas said: “These exciting findings represent a major step forward for dementia research and could herald a new era for people with Alzheimer’s disease.
“This is the first time a drug has been shown to both reduce the disease in the brain and slow memory decline in clinical trials.”
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The new drug works by targeting amyloid protein, a sticky substance associated with the onset of Alzheimer’s. Lecanemab, an engineered antibody, latches on to the protein and attracts immune cells, which then break down the protein deposit.
In the clinical trial, 1795 volunteers identified as having early-stage Alzheimer’s were given fortnightly infusions of lecanemab. The volunteers were split into two groups, with 898 receiving lecanemab and 897 a placebo.
The trial found that lecanemab “reduced markers of amyloid in early Alzheimer’s disease and resulted in moderately less decline on measures of cognition and function than placebo at 18 months”.
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Is this a genuinely “historic” breakthrough?
The best way to answer that question is ‘yes and no’. In the context of comparison with previous trials, it is certainly a breakthrough. Numerous trials have failed to find a drug that makes any difference at all, according to Professor Tara Spires-Jones, from the University of Edinburgh.
She said the new results were “a big deal because we’ve had a 100 per cent failure rate for a long time”.
Dr Kohlhaas says the trial has produced “modest results”. Those who received lecanemab showed a 0.45 point advantage over those who didn’t, using an 18-point scale ranging from normal through to severe dementia.
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That does seem to be modest. Part of the reason is likely to be that amyloid protein is only one marker of Alzheimer’s.
Another toxic protein, tau, has been found where brain cells are dying, and some researchers, Prof. Spires-Jones included, believe that is more likely to be involved with the onset of the disease.
Nevertheless, the results are an important milestone in the search for an Alzheimer’s cure. According to Prof. Spires-Jones, the findings put researchers “on the cusp of understanding enough to get a hold of the problem and we should have something that will make a bigger difference in a decade or so”.
Health regulators in the US, who will soon decide whether lecanemab can be approved for wider use, and pharmaceutical companies Eisai and Biogen – who developed the drug – plan to begin the approval process in other countries next year.
Has someone in your family been diagnosed with dementia? Has he or she had any success with existing drugs? Why not share your thoughts in the comments section below?
