- The first drug to slow the destruction of the brain in Alzheimer’s has been heralded as momentous.
- The research breakthrough ends decades of failure.
- Yet the medicine, lecanemab, has only a small effect.
Lecanemab attacks the sticky gunge – called beta amyloid – that builds up in the brains of people with Alzheimer’s. For a medical field littered with duds, despair and disappointment, some see these trial results as a triumphant turning point.
Momentous Event
Alzheimer’s Research UK said the findings were “momentous”. One of the world’s leading researchers behind the whole idea of targeting amyloid 30 years ago, Prof John Hardy, said it was “historic” and was optimistic “we’re seeing the beginning of Alzheimer’s therapies”. Prof Tara Spires-Jones, from the University of Edinburgh, said the results were “a big deal because we’ve had a 100% failure rate for a long time”.
Currently, people with Alzheimer’s are given other drugs to help manage their symptoms, but none change the course of the disease. Lecanemab is an antibody – like those the body makes to attack viruses or bacteria – that has been engineered to tell the immune system to clear amyloid from the brain. Amyloid is a protein that clumps together in the spaces between neurons in the brain.
The large-scale trial involved 1,795 volunteers with early stage Alzheimer’s. Infusions of lecanemab were given every fortnight. The data is already being assessed by regulators in the US who will soon decide whether lecanemab can be approved for wider use.
Will It Make a Difference ?
There is debate among scientists and doctors about the “real world” impact of lecanemab. The slower decline with the drug was noticed using ratings of a person’s symptoms. It’s an 18-point scale, ranging from normal through to severe dementia. Those getting the drug were 0.45 points better off.
Dr Susan Kohlhaas, from Alzheimer’s Research UK, said it was a “modest effect… but it gives us a little bit of a foothold” and the next generation of drugs would be better. There are also risks. Brain scans showed a risk of brain bleeds (17% of participants) and brain swelling (13%). It is even scientifically plausible that the effectiveness could be greater in longer trials. “I don’t think we can assume that this is it,” says Dr Kohlhass.
The emergence of drugs that do alter the course of the disease asks big questions of whether the health service is ready to use them. The Alzheimer’s Society says more than 850,000 people in the UK have some form of dementia. More than half have Alzheimer’s, but everyone would need testing. The immune system and inflammation are heavily involved in the disease and another toxic protein called tau is the one that’s found where brain cells are actually dying. Speaking to Radio 4’s Today programme, Kate Lee, chief executive of Alzheimer’s Society charity, said Lecanemab would not have a “huge impact” on those who already live with dementia. But she added it should “make a big difference” for future generations.”
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Source: BBC
