Home News Lecanemab, an Alzheimer’s medication, is heralded as a major development.

Lecanemab, an Alzheimer’s medication, is heralded as a major development.

It has been hailed as historic that the first medication to reduce Alzheimer’s brain deterioration has been developed.

The scientific discovery puts a stop to decades of futility and demonstrates that new drug development for Alzheimer’s, the most prevalent form of dementia, is feasible.

Lecanemab, however, has a negligible impact on people’s daily lives, and its relevance is up for question.

Without a revolution in illness detection, most people would miss out on the drug’s benefits because it only acts in the early stages of the disease.

Lecanemab targets the beta-amyloid, a sticky gunge that accumulates in Alzheimer’s patient’s brains.

Some view the outcomes of this research as a successful turning point in a medical sector plagued with failures, sorrow, and disappointment.

The results, according to Alzheimer’s Research UK, were “momentous.”

Prof. John Hardy, one of the pioneering scientists who proposed the notion of focusing on amyloid 30 years ago, called it “historic” and expressed hope that “Alzheimer’s medicines are starting to emerge.” We’ve had a 100% failure rate for a very long time, so the results are “a major thing,” according to Prof. Tara Spires-Jones of the University of Edinburgh.

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Other medications are currently prescribed to Alzheimer’s patients to assist manage their symptoms, but none of them alter the course of the illness.

Lecanemab is a designed antibody that instructs the immune system to remove amyloid from the brain. Antibodies are made by the body to combat viruses and germs.

Lecanemab, an Alzheimer's medication, is heralded as a major development.
Lecanemab, an Alzheimer’s medication, is heralded as a major development.

One of the distinguishing features of Alzheimer’s is the formation of amyloid plaques, which are formed when the protein amyloid collects in the gaps between neurons in the brain.

A total of 1,795 individuals with early-stage Alzheimer’s participated in the extensive trial. Every two weeks, Lecanemab infusions were administered.

The findings, which were presented at the Clinical Trials on Alzheimer’s Disease conference in San Francisco and reported in the New England Journal of Medicine, do not represent a magical treatment. Although the disease continued to sap people’s mental capacity, the 18 months of treatment decreased that loss by around a fifth.

Regulators in the US are already reviewing the data and will make a decision soon on whether Lecanemab can be used more widely. Next year, the developers—the pharmaceutical firms Eisai and Biogen—plan to start the approval procedure in other nations.

David Essam, who is 78 and from Kent in the UK, took part in the international trial.

His Alzheimer’s meant he had to give up work as a joiner – he could no longer remember how to build a cabinet or use his tools. He now uses a digital watch as he can’t tell time using a clock face.

“He’s not the man he was, he needs help with most things, and his memory in general is almost non-existent,” said his wife Cheryl. But she said the trial had given the family hope.

It’s simply an awful, nasty thing, said David, and if someone can slow it down and finally stop it altogether, that would be fantastic.

David is one of more than 55 million individuals around the world who have Alzheimer’s disease, and by 2050, that figure is expected to rise to more than 139 million.

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.

There are also risks. Brain scans showed a risk of brain bleeds (17% of participants) and brain swelling (13%). Overall, 7% of people given the drug had to stop because of side effects.

What happens after the 18-month experiment is a vital subject, and the answers are still up for debate.

Patients at North Bristol NHS Trust are seen by Dr. Elizabeth Coulthard, who claims that once moderate cognitive impairment begins, people can live independently for an average of six years.

She argues that if the decrease is slowed by 25%, that may translate to an additional 19 months of independent living, “but we don’t know that yet.”

Even from a scientific perspective, it is conceivable that lengthier studies might yield larger results. Dr. Kohlhass says, “I don’t think we can presume that this is it.

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 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 to come forward at the earliest signs of memory problems and doctors able to send them for amyloid tests – either brain scans or spinal fluid analysis – to a determination if they have Alzheimer’s or another form of dementia. At the moment only 1-2% of people with dementia have such tests.

“There’s an enormous gulf between current service provision and what we need to do, to deliver disease-modifying therapies,” said Dr Coulthard.

She said that, currently, only those living near big medical centers or paying privately were likely to benefit.

Scientists also stressed that amyloid was only one part of the complex picture of Alzheimer’s disease and should not become the sole focus of therapies.

The immune system and inflammation are heavily involved in the disease and another toxic protein called tau is one that’s found where brain cells are actually dying.

“That’s where I would put my money,” said Prof Spires-Jones.

She added: “I’m very excited we’re on the cusp of understanding enough to get a hold of the problem and we should have something that will make a bigger difference in a decade or so.”

source: summarybio.com