Lecanemab: Experimental Alzheimer’s drug has ‘historic’ results

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For the first time, a drug has shown itself capable, in experiments with volunteers, of slowing down the destruction of the brain by Alzheimer’s disease.

The success of the research, disclosed this Tuesday (29/11) in the scientific journal New England Journal of Medicine, ends decades of failures in experimental treatments against Alzheimer’s, the most common form of dementia.

However, the drug, lecanemab, still showed some limitations: its effect was moderate and it carried some risks. Imaging exams showed the occurrence of cerebral hemorrhages in 17% of the participants and cerebral swelling in 13%. Among the volunteers, 7% had to leave the tests due to side effects.

Lecanemab attacks the sticky goo that builds up in the brains of people with Alzheimer’s, called beta-amyloid. The drug works in the early stages of the disease, so most people would not benefit from it, as the condition is often only investigated after signs appear – often in relatively advanced stages.

British research center Alzheimer’s Research UK said the results were “important”.

One of the first researchers in the world to propose treatments that target amyloid, more than 30 years ago, Professor John Hardy evaluated that the experiment is “historic” and shows that “we are seeing the beginning of treatments against Alzheimer’s”.

Professor Tara Spiers-Jones from the University of Edinburgh said the results were “important because we’ve had a 100% failure rate for so long”.

Currently, people with Alzheimer’s are given drugs to control their symptoms, but none change the course of the disease directly.

Lecanemab is an antibody — like those the body makes to attack viruses or bacteria — designed 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 plaques that are very characteristic of Alzheimer’s disease.

The large-scale study involved 1,795 volunteers with early-stage Alzheimer’s disease. Lecanemab infusions were given biweekly.

The results, presented at the Clinical Trials on Alzheimer’s Disease conference in San Francisco, United States, do not reveal a miracle cure. The disease continued to deteriorate people’s brain functions, but that decline was slowed by about a quarter over the 18 months of treatment.

The data is already being evaluated by US regulators, who will soon decide whether lecanemab can be approved for wider use. The drug’s developers, pharmaceutical companies Eisai and Biogen, plan to apply for such permission next year in other countries.

David Essam, who is 78 years old and from Kent, UK, took part in the clinical trials.

Illness forced him to give up work as a carpenter—he no longer remembered how to use his tools or build a cupboard. He now wears a digital watch as he cannot tell time using an analog watch.

“If anyone can slow down [o Alzheimer] and eventually stopping it altogether would be brilliant. It’s just a horrible thing,” says David, referring to the disease.

His wife, Cheryl, laments already very noticeable changes in her husband, but says that participating in the clinical trials has brought hope to the family.

“He’s not the man he once was. He needs help with most things and generally his memory is almost gone,” says his wife.

There are more than 55 million people in the world like David and the number of people with Alzheimer’s disease is expected to exceed 139 million by 2050, according to projections.

Limitations

There is debate among scientists and clinicians about the impact of lecanemab in the “real world”.

The best results were found in individual symptom assessments. It is an 18-point scale, ranging from normal to severe dementia. Those who received the drug scored 0.45 points higher.

Professor Tara Spiers-Jones said a “small effect” of the drug on the disease has been seen, but “even if it’s not something that impactful, I would accept it”.

Susan Kohlhaas, from Alzheimer’s Research UK, said it was a “modest effect, but one that gives us some ground.” For her, the next generation of drugs against Alzheimer’s must be better.

A crucial question is what will happen after the 18 months of the experiment, and the answers are still speculation.

Dr Elizabeth Coulthard, who treats patients in Bristol’s public health network, says people have, on average, six years of independent life since mild cognitive impairment begins.

If the decline is reduced by a quarter, as seen in clinical trials, that would give an additional 19 months of independent living — but for now, that’s just a guess, she says.

It is even scientifically plausible that the effectiveness could be greater in longer trials.

The emergence of drugs that alter the course of the disease raises big questions about whether health services are ready to use them.

The drugs must be given early in the disease, before too much brain damage occurs, but a very small percentage of people are screened early to detect Alzheimer’s.

“There is a huge gulf between the care provided today and what we need to do to deliver treatments that alter the course of the disease,” says Coulthard.

Some scientists have also emphasized that amyloid is just one piece in the complex picture of Alzheimer’s disease and should not be the sole focus of therapies.

The immune system and inflammatory processes are heavily involved in the disease, as well as another toxic protein called tau — found where brain cells are actually dying.

“That’s where I’d put my money,” Spiers-Jones opines. “I am very excited that we are on the verge of understanding the problem sufficiently. We should have something [tratamento] that will make a bigger difference in a decade or so.”

*This text was published at https://www.bbc.com/portuguese/geral-63803472

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