The first drug to slow the destruction of the brain in Alzheimer’s has been heralded as historic.
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 disappointment, some see these trial results as a triumphant turning point. 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”.
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 and forms distinctive plaques that are one of the hallmarks of Alzheimer’s.
The large-scale trial involved 1,795 volunteers with early stage Alzheimer’s. Infusions of lecanemab were given every fortnight.
The results of the Clinical Trials are not a miracle cure. The disease continued to rob people of their brain power, but that decline was slowed by around a quarter over the course of the 18 months of treatment.
The data is already being assessed by regulators in the US who will soon decide whether lecanemab can be approved for wider use. The developers – the pharmaceutical companies Eisai and Biogen – plan to begin the approval process in other countries next year.
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. Prof Spires-Jones said that was a “small effect” on the disease, but “even though it is not dramatic, I would take it”.
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.
A crucial question is what happens after the 18 months of the trial, and the answers are still speculation.
Dr Elizabeth Coulthard, who treats patients at North Bristol NHS Trust, says that people have, on average, six years of living independently once mild cognitive impairment starts.
“Slow that decline by a quarter and it could equate to an extra 19 months of independent life, “but we don’t know that yet”, she says.
The drugs have to be given early in the disease before too much damage to the brain is done, whereas most people referred to memory services are in the later stages of the disease.
That requires people coming forward at the earliest signs of memory problems and doctors being able to send them for amyloid tests – either brain scans or spinal fluid analysis – to determine if they have Alzheimer’s or another form of dementia.
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.
Kate Lee, chief executive of Alzheimer’s Society charity, called for a 10-year government strategy on dementia to deal with what she called the “biggest health crisis we face in the UK”.
Speaking to Radio 4’s Today programme, she also 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.
