Lecanemab, an Alzheimer’s medication, heralded as a major advancement

The first medication to reduce Alzheimer’s-related brain damage has been hailed as historic.

The scientific discovery puts a stop to decades of disappointment and suggests that Alzheimer’s disease, the most prevalent kind of dementia, may be treated with new medications.

However, the influence of the medication lecanemab on people’s day-to-day life is debatable and has a very limited effect.

Furthermore, most people would not benefit from the medication if early illness detection weren’t revolutionized.

Lecanemab targets the beta amyloid, a sticky substance that accumulates in the brains of Alzheimer’s patients.


Some regard the outcomes of these trials as a victorious turning point in a medical sector bereft of failures, hopelessness, and disappointment.

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“Momentous” was how Alzheimer’s Research UK described the results.

Prof. John Hardy, one of the top scientists in the world who spearheaded the concept of focusing on amyloid thirty years ago, called it “historic” and expressed optimism that “we’re seeing the beginning of Alzheimer’s therapeutics.” The University of Edinburgh’s Prof. Tara Spires-Jones called the outcomes “a major thing since we’ve had a 100% failure rate for a long time.”

Presently, additional medications are prescribed to Alzheimer’s patients to assist control their symptoms; nevertheless, none of these alter the course of the illness.

Lecanemab is an antibody designed to instruct the immune system to remove amyloid from the brain. Antibodies like these are produced by the body to combat germs or viruses.

One of the defining features of Alzheimer’s disease is the formation of characteristic plaques, which are caused by the protein amyloid clumping together in the areas between brain neurons.

1,795 individuals in the large-scale experiment had Alzheimer’s disease in the early stages. Every two weeks, lecanemab infusions were administered.

The findings, which were published in the New England Journal of Medicine and presented at the Clinical Trials on Alzheimer’s Disease conference in San Francisco, do not provide a miraculous treatment. Over the course of the 18 months of therapy, the illness did not stop robbing people of their mental capacity; nevertheless, this decrease was delayed by around 25%.

US officials are currently reviewing the data and will make a decision shortly about the approval of lecanemab for broader use. The pharmaceutical firms Eisai and Biogen, who are the creators, want to start the approval procedure in additional nations early in 2019.

The 78-year-old Kent, UK resident David Essam participated in the worldwide trial.

Due to his Alzheimer’s, he was unable to continue working as a joiner since he could not recall how to operate his equipment or construct a cabinet. He can’t tell time using a clock face, therefore he now wears a digital watch.

His wife Cheryl said of him, “He’s not the guy he was, he requires help with most things, his memory in general is basically non-existent.” The family, she claimed, now had hope because of the trial.

“It’s simply an awful unpleasant thing,” David stated, “if anyone can slow it down and finally stop it all together that would be fantastic.”

David is one of over 55 million individuals worldwide who have Alzheimer’s disease, and by 2050, there will be over 139 million cases of the condition.

Does it really matter?

Physicians and scientists disagree on how lecanemab will affect patients in the “real world.”

The drug’s slower fall was observed when a person’s assessments of their symptoms were used. There are eighteen points on the scale, from mild dementia to severe dementia. The benefit to those receiving the medication was 0.45 points.

It is a “modest effect” on the illness, according to Prof. Spires-Jones, but “even if it is not dramatic, I would accept it.”

It’s a “small impact… but it offers us a little bit of a footing,” according to Dr. Susan Kohlhaas of Alzheimer’s Research UK, who also claimed that the upcoming medication generation will be superior.


Additionally, there are dangers. Brain bleeding (17%) and brain swelling (13%), according to brain scan results, were possible outcomes. Overall, adverse problems forced 7% of those prescribed the medication to discontinue.

What transpires over the trial’s 18 months is a key topic, and the answers are still up for debate.

Patients treated by Dr Elizabeth Coulthard of the North Bristol NHS Trust often live freely for six years after the onset of moderate cognitive impairment.

“But we don’t know that yet,” she adds. If we can slow that decrease by a quarter, that may add up to an additional 19 months of independent life.

It is also conceivable from a scientific standpoint that lengthier trials might yield higher efficacy. Dr. Kohlhass says, “I don’t think we can presume that this is all.”

The advent of medications that can really change the course of the illness raises important concerns about the health service’s readiness to employ them.

While most patients referred to memory services are in the latter stages of the disease, the medications must be started early in order to prevent too much brain damage.

In order to ascertain if a patient has Alzheimer’s disease or another type of dementia, it is necessary for individuals to come forward at the first indications of memory issues and for clinicians to be able to refer them for amyloid testing, which can involve brain scans or spinal fluid analysis. Currently, only 1% to 2% of dementia patients receive these testing.

According to the Alzheimer’s Society, around 850,000 individuals in the United Kingdom suffer with dementia. Though testing would be necessary for everyone, more than half have Alzheimer’s.

Dr. Coulthard stated, “There’s a huge gap between what we need to do to offer disease-modifying treatments and what we now provide.”

Currently, she claimed, the only people likely to gain were those who paid privately or lived close to large medical facilities.

Additionally, researchers emphasized that amyloid should not be the only focus of treatment as it is only one aspect of the intricate picture of Alzheimer’s disease.

The illness is mostly mediated by the immune system and inflammation, and the tau protein—another harmful protein—is present in the areas of the brain where brain cells are really dying.

“I would invest my money there,” Prof. Spires-Jones stated.

“I’m really pleased that we’re about to grasp the problem well enough to have something that will make a greater difference in a decade or two,” she continued.

The head of the Alzheimer’s Society organization, Kate Lee, has asked for a 10-year plan to address dementia, referring to it as the “greatest health problem we face in the UK.”

She said that lecanemab wouldn’t have a “big impact” on people who already have dementia in an interview with Radio 4’s Today program.

It should, however, “make a tremendous impact” for coming generations, she continued.

Source:
https://www.bbc.com/news/health-63749586

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