Researchers have announced the very first drug that slows brain destruction in Alzheimer’s patients, thought it is still in the early stages of development.
The drug known as lecanemab is part of a new era of drugs for treating Alzheimer’s, a common form of dementia. These drugs remove clumps of protein called beta amyloid that builds up in the brain.
Lecanemab is now attaining credibility after decades of failure in the field. Encouraged experts note that Alzheimer’s, which affects over thirty million people worldwide, could finally be treatable.
Although the drug has a notably small effect and its impact on people’s daily lives is still questionable, some see these trial results as a triumphant turning point for Alzheimer’s patients.
Bart De Strooper, director of the UK Dementia Research Institute at University College London, said, “This is the first drug that provides a real treatment option for Alzheimer’s patients.”
Professor John Hardy, one of the world’s leading researchers behind the whole idea of targeting amyloid thirty years ago also said it was “historic.” He is optimistic “we’re seeing the beginning of Alzheimer’s therapies.”
Professor Tara Spires-Jones of the University of Edinburgh said the results were “a big deal because we’ve had a 100 [percent] failure rate for a long time.”
Current drugs for Alzheimer’s presented no change on patients
Although patients with Alzheimer’s are currently being administered other drugs to help manage symptoms, none has posed any change to the course of the disease.
However, lecanemab is an antibody—much like those the body makes to attack viruses or bacteria. It has been engineered to tell the immune system to clear amyloid from the brain and has portrayed decline—albeit slow—in a large-scale trial.
In fact, results from trials involving 1,795 volunteers with early stage Alzheimer’s, which were presented at the Clinical Trials on Alzheimer’s Disease conference in San Francisco and published in The New England Journal of Medicine, indicated that the drug reduced the decline in patients’ overall mental skills by twenty-seven percent over eighteen months.
Nick Fox, professor of clinical neurology and director of the Dementia Research Centre at UCL, said, “I believe it confirms a new era of disease modification for Alzheimer’s disease.”
“An era that comes after more than 20 years of hard work on anti-amyloid immunotherapies, by many, many people, and many disappointments along the way,” he added.
The data, however, is already being assessed by regulators in the US who will soon decide whether lecanemab can be approved for wider use. Lecanemab developers, the pharmaceutical companies Eisai and Biogen, are planning to begin the approval process in other countries next year.
Magnitude at which Alzheimer’s affects the world
According to statistics, Alzheimer’s accounts for nearly two-thirds of the fifty-five million people living with dementia worldwide, and the disease is projected to exceed 139 million people by 2050.
Actually, it is the leading cause of death in the UK, and it amounts to a cost of over thirty billion dollars a year, with patients typically dying within seven years of a diagnosis.
The most common early sign is memory problems, but, as the disease progresses, people can find themselves lost in familiar places, having trouble with decisions, struggling with simple tasks, and ultimately unable to eat or move without help.
According to David Essam, a 78-year-old from Kent in the UK who took part in the international trial, his Alzheimer’s meant he had to give up work as a joiner because he could no longer remember how to build a cabinet or use his tools.
Essam is currently using a digital watch because 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.
David said, “If somebody can slow [Alzheimer’s] down and eventually stop it all together that would be brilliant…[because] it’s just a horrible nasty thing.”
Is the drug a fully dependable remedy to brain destruction?
According to Dr. Susan Kohlhaas from Alzheimer’s Research UK, lecanemab had a “modest effect…but it gives us a little bit of a foothold,” and the next generation of drugs can be expected to be better.
Dr. Kohlhaas’ observation adds to the huge 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 eighteen-point scale ranging from normal through to severe dementia, and those getting the drug were 0.45 points better off.
Spires-Jones also noted that it has a “small effect” on the disease, but “even though it is not dramatic, I would take it.”
However, in brain scans, certain side effects were detected. These included a risk of brain bleeds in seventeen percent of participants and brain swelling in thirteen percent of individuals. Hence, overall, seven percent of people administered the drug had to stop taking it because of these side effects.
Furthermore, questions have been raised about the drug’s safety after the deaths of two individuals on the trial were linked to the drug by some researchers.
According to the published report, thirteen people died on the trial. Six of them received the drug, while seven received the placebo. The report states that none of the deaths were considered by investigators to be related to the drug.
Jonathan Schott, professor of neurology at UCL and chief medical officer at Alzheimer’s Research UK, said, “Lecanemab is not a panacea, but it provides proof of concept that Alzheimer’s is not an impossible problem: it is potentially treatable and perhaps one day even preventable.”
“We need to expand our research, and to continue to investigate different drugs targeting different aspects of the disease,” he said. “Ultimately it is likely that combination therapies will be needed.”
Other shortfalls to the Alzheimer’s drug
Besides the medical shortfalls currently attributed to this Alzheimer’s drug, it is uncertain when and even whether it will be approved by the UK’s Medicines and Healthcare products Regulatory Agency and the National Institute for Health and Care Excellence (NICE).
Even prior to approval, the drug is expensive, costing between twelve to sixteen thousand dollars per patient a year in the United Kingdom.
Another issue is that the NHS is not equipped to deliver the drug because it lacks sufficient diagnostic tests to identify those most likely to benefit. There is also low staff turnover which would make administering drug infusions to patients every two weeks challenging.
Lastly, the NHS apparently cannot provide the multiple MRI scans needed throughout treatment to check for side effects, such as brain swelling and hemorrhages.
At this time, it is crucial to think about what comes after the eighteen month-trial, as this remains unclear.