The fight against Alzheimer’s disease has been one of the most difficult tasks of medical science for many years. Therefore, it is not surprising that a new drug that slows down memory loss caused a lot of excitement.
Lecanemab appears to slow disease progression by 27 percent and is hailed by some experts as welcome evidence that Alzheimer’s can be treated.
Far from being a cure for a disease, it comes with its own health warnings, not the least of which is the potential for unpleasant side effects, but it represents a potential breakthrough in the search for treatments.
“I really believe this is the beginning of the end,” said Professor Sir John Hardy, team leader at the UK’s Dementia Research Institute at University College London (UCL), when the results of the clinical trial were published in New England Journal of Medicine.
The drug is designed to attack and remove amyloid, a protein that accumulates in the brains of people with Alzheimer’s disease and is the focus of treatment searches.
The “amyloid hypothesis” arose 30 years ago from the suggestion that the processes that control the production, accumulation, or removal of beta-amyloid could be the key to discovering treatments or even cures. Lecanemab is an antibody that attaches to amyloid, causing it to be removed from the brain by the immune system.
“It’s amazing to get this confirmation that we’ve been on the right track all this time,” Professor Hardy said.
His hopes are understandable, as his research has revealed for the first time the role of amyloid as the cause of Alzheimer’s disease, and of those whose life’s work is to find a cure for a disease that will afflict more than 1 million people by the end of the century. will meet us. Decade. But he was one of the first to admit that the development of a new drug, although encouraging, is more of a beginning than an end.
“The first step is the most difficult, and now we know exactly what we need to do to develop effective drugs. It’s good to think that future work will build on this and that we will soon have life-changing methods of dealing with this disease,” said Professor Hardy.
Over the past three decades, scientists have suffered many setbacks trying to find cures that could improve the lives of people with Alzheimer’s disease, a disease that will affect a million people in the UK by the end of the decade.
While praising the results of the lekanemab study, a 27 percent reduction in memory loss attracted media attention. On average, people with mild cognitive impairment live on their own for six years. If this decline is slowed by a quarter with lekanemab, this could theoretically lead to an additional 19 months of independent living, but it is too early to tell if this will actually happen and only time and further research will demonstrate this.
Areas of concern also need further study before they can be approved for widespread use. Possible side effects include stroke, which raises concerns that it may be too dangerous to use.
People with Alzheimer’s disease are currently prescribed other medications to control their symptoms, but none of them change the course of the disease. Lecanemab may be able to do this if longer-term studies determine the efficacy and safety of the drug in the early stages of Alzheimer’s disease.
Professor Hardy said: “It is still a long way before these drugs are approved and used in standard clinical practice, but this is certainly the first phase.”
The National Health Service must also be ready to provide patients with new treatments for Alzheimer’s when the time comes. It is important that drugs be given early in the disease, before too much brain damage is done. Currently, most people who seek help from memory services are in the later stages of the disease because too few people report memory problems at the first sign.
General practitioners should also be able to refer such patients for amyloid tests – brain scans or spinal fluid tests – to determine if they have Alzheimer’s disease or some other form of dementia. Currently, only 1-2 percent of people with dementia have such tests. Dementia diagnosis rates must improve or people will be denied access to potentially life-changing drugs if and when they become available.
Eisai said the results of the lekanemab study “proved” the amyloid hypothesis, but most scientists believe that amyloid is only part of the complex picture of Alzheimer’s disease and should not be the only avenue of therapy.
Another toxic protein, called tau, is found where brain cells die, and researchers would like it not to be ignored just because of its success with amyloid.
“I think lekanemab has resurrected the idea that you can now create a combination of amyloid(s) and tau,” the doctor said. Reisa Sperling, neurologist and Alzheimer’s disease researcher at Harvard Medical School. “We’ve been trying to do combination tests for years.”
Nearly a decade ago, Alzheimer’s experts gathered in Washington to discuss attempts at combination therapy, but “no one wanted to listen,” Dr. Wilson said. Sparrow.
Dr. Spurling and other researchers at the Alzheimer’s Disease Clinical Trials Consortium (ACTC), a research network supported by the National Institute on Aging in the US, now say drug makers are increasingly interested in participating in a trial to test tau drugs alone and in combination. identify the exam. with anti-amyloid drugs such as lecanemab.
All of a sudden everyone is interested and the group is expecting a funding response by the end of the year.
While several antibody therapies designed to slow tau accumulation failed completely in the past year, and Roche’s drug, semorinemab, has shown limited effectiveness, new trials of tau drugs will focus on building on the advances of lekanemab – using brain scans, spinal fluid and blood tests for a better evaluation. the stage of the disease, when to intervene and whether the drug achieves its goal. This would allow companies to test drugs before symptoms appear.
Several pharmaceutical companies, including Roche, Merck, Johnson & Johnson and Eli Lilly, are working on tau-targeting therapies. At least 16 therapies are currently in clinical trials with results expected within the next three years. “The understanding of disease is getting a lot better,” said Jason Uslaner, head of Discovery Neuroscience at Merck.
The World Health Organization (WHO) has pushed back the deadline for finding a cure for Alzheimer’s disease – the most common form of dementia – from 2025 to 2030, stressing how difficult it is to make progress. An earlier deadline was set at the G8 Dementia Summit in 2013.
Since dementia is caused by several diseases, it is unlikely that there will be a single cure, but lekanemab has shown that an effective treatment will someday be possible.
Professor Tara Spears-Jones, Program Director of the British Dementia Research Institute and Associate Director of the Center for Brain Research at the University of Edinburgh, said: [the lecanemab study] Good news from a well-conducted study, it’s important to note that this is not a cure. Longer-term studies are needed to make sure the benefits of this treatment outweigh the risks.
“As a scientist who has studied Alzheimer’s disease for many years, I am very pleased that years of basic neuroscience research have led to treatments that can slow the progression of Alzheimer’s disease and reverse some of the pathological changes in the brain. This discovery will stimulate research and provide hope that treatments based on ongoing neuroscience research will only get better.”
Source: I News
I’m Raymond Molina, a professional writer and journalist with over 5 years of experience in the media industry. I currently work for 24 News Reporters, where I write for the health section of their news website. In my role, I am responsible for researching and writing stories on current health trends and issues. My articles are often seen as thought-provoking pieces that provide valuable insight into the state of society’s wellbeing.