A first-of-its-kind Alzheimer’s drug that slows cognitive decline in early-stage patients, that was developed using animal research, has now been licensed for use around the world, including China, Japan, USA and most recently in the UK.
Lecanemab is the first Alzheimer’s drug that directly targets aspects of the disease itself, rather than just the symptoms. It works by removing an abnormal build-up of beta-amyloid proteins in the brain, which have been implicated in Alzheimer's.
The drug, an antibody derived from mice, highlights the long-standing role of animal research in its development and approval.
Before being tested in humans, studies in mice showed that lecanemab could work by reaching the brain, specifically binding to beta-amyloid and successfully protecting neurons.
As a humanised mouse antibody – that is made to be more ‘human-like’ so it does not trigger an immune reaction in people – lecanemab can recognise and bind to the amyloid proteins in human patients.
One clinical trial showed that it reduced beta-amyloid levels and slowed cognitive decline by 27%.
It was also originally thanks to studying genetically modified mice, that researchers first understood the toxic effect that beta-amyloid can have in Alzheimer’s disease.
The UK Alzheimer’s Society said in a recent statement that the drug approval was 'a defining moment for people with early-stage Alzheimer’s disease in the UK and a significant step towards a more hopeful future'.
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Lecanemab is the first Alzheimer's medication that specifically addresses elements of the illness itself, rather than only attempting to drift hunters alleviate the symptoms. Its mechanism of action involves the elimination of an aberrant accumulation of beta-amyloid proteins in the brain, which have been associated with Alzheimer?s disease.
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