- James Gallagher
- Health and science journalist
Licanib is an antibody designed to tell the immune system to clear amyloid from the brain
The announcement of the first drug effective in slowing brain damage resulting from dementia (Alzheimer’s disease) was highly celebrated by the medical community, which considered it an historic and important moment.
This research breakthrough is set to end decades of failure and demonstrate that a new era of drugs is possible to treat Alzheimer’s disease, the most common form of dementia.
Despite this, the drug, called lecanimab, has only a small effect and its impact on people’s daily lives is still a matter of debate.
The drug works in the early stages of the disease, so most patients won’t benefit from the new discovery unless methods of early detection are developed.
Licanib attacks the sticky substance called beta amyloid (beta-amyloid peptide) that builds up in the brains of people with Alzheimer’s disease.
For a medical field filled with failure, despair and disappointment, some see these achievements as a triumphant breakthrough.
Alzheimer’s Research UK has confirmed the findings are “hugely significant”.
It is “historic” and encouraging, said Professor John Hardy, one of the world’s leading researchers behind the whole idea of targeting amyloid 30 years ago, “we are seeing the beginning of treatments for Alzheimer’s”.
Professor Tara Spears-Jones, from the University of Edinburgh, said the results were significant, ‘because we’ve had a 100% failure rate over a long period of time’.
Currently, Alzheimer’s patients are given other medications to help manage their symptoms, but nothing changes the course of the disease.
Licanib is an antibody, such as that made by the body to attack viruses and bacteria, designed to tell the immune system to clear the amyloid from the brain.
Amyloid is a protein that collects in the spaces between nerve cells in the brain and forms special plaques that are one of the hallmarks of Alzheimer’s disease.
The drug was tested on a large scale with the participation of 1,795 volunteers suffering from Alzheimer’s disease in its early stages. Lekanimab was administered every two weeks.
The findings were presented at the Alzheimer’s Clinical Trials Conference in San Francisco and published in the New England Journal of Medicine, but they’re not a magic cure. Symptoms of the disease continued to deprive people of their mental abilities, but this decline slowed by about a quarter over the course of 18 months of treatment.
The data is already being evaluated by US regulators, who will soon decide whether licanib can be approved for wider use. The drug’s developers, Japan’s Eisai Corp. and US Biogen Pharmaceuticals, plan to get the drug approved in other countries next year.
David Essam, 78, who was in Great Britain, took part in international trials of the drug.
Issam suffers from Alzheimer’s, had to give up working as a carpenter and no longer remembers how to make a wardrobe or how to use his tools. He now he uses a digital clock because he can’t tell the time using a normal clock.
His wife Cheryl said, “He’s not the man he was, he needs help with most things and his memory in general is almost non-existent.” But she said the experience gave the family hope.
“If someone can slow down[Alzheimer’s disease]and eventually stop it, that would be great, because it’s just a bad disease,” Essam said.
There are more than 55 million people in the world like David Essam, and the number of people with Alzheimer’s disease is projected to exceed 139 million by 2050.
Will it make a difference?
There is debate among scientists and physicians about the effect of licanib in the ‘real world’.
Slowing the memory decline with the drug was monitored by assessing the person’s symptoms. The investigators set up an 18-point scale, ranging from normal dementia to severe dementia. Those who received the drug were 0.45 points better.
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The emergence of disease-altering drugs raises big questions about whether health services are ready to use them
Professor Spiers-Jones said it had a ‘little effect’ on the disease, but ‘although not significant, I would accept it’.
Dr Susan Koolhaas, from Alzheimer’s Research UK, said it was a ‘modest effect … but it gives us a bit of an edge’, and the next generation of drugs will be even better.
But there are also risks associated with the drug. Brain scans showed a risk of brain hemorrhage (17% of participants) and brain swelling in 13%. Overall, 7% of people who took the drug had to stop due to side effects.
The crucial question is what will happen 18 months after the experiment and the answers are still speculation.
Dr Elizabeth Coulthard, who treats patients in North Bristol, says people have an average of six years of independent living once MCI sets in.
He added that working to slow this decline by a quarter could be equivalent to an additional 19 months of independent living without needing assistance, “but we don’t know that yet.”
It’s even scientifically plausible that efficacy is higher in longer trials. “I don’t think we can assume that will happen,” says Dr. Koolhaas.
The emergence of disease-altering drugs raises big questions about whether health services are prepared to use them.
Drugs must be given early in the disease before significant brain damage occurs, while most people who are referred to memory services are in the later stages of the disease.
This requires people to apply for treatment as soon as they develop signs of memory problems and for doctors to be able to give them amyloid tests, with brain scans or spinal fluid tests, to determine if they have Alzheimer’s disease or another form of dementia. .
Currently, only 1-2% of people with dementia undergo such tests.
“There is a huge gap between current service delivery and what we need to do to deliver disease-modifying therapies,” said Dr. Elizabeth Coulthard.
For now, he added, only those who live near large medical centers or pay private money are likely to benefit.
The scientists also emphasized that amyloid is only one part of the complex picture of Alzheimer’s disease and should not become the sole target of treatments.
The immune system and inflammation are heavily involved in the disease, and another toxic protein called tau is found where brain cells are already dying.
‘Here’s where it’s worth it,’ said Professor Spiers-Jones.
“I’m really excited that we’re on the cusp of understanding enough to work around this and should have something that makes a bigger difference in a decade or so,” he added.
