This is Everyday Science with Clare Wilson, a subscriber-only newsletter from The i Paper. If you’d like to get this direct to your inbox every week, you can sign up here.
Hello, and welcome back to Everyday Science.
When the NHS rejected two new treatments for Alzheimer’s disease last year on the grounds that they are not cost-effective, medical charities and some doctors branded the decision a blow to patients. But this week, an independent review has found that the drugs don’t deliver any worthwhile benefits.
Why can’t experts agree on whether the drugs work or not – and what are the other options for patients and their families?
New treatments for Alzheimer’s are certainly needed. The condition, which causes memory loss and confusion, is the most common form of dementia and case numbers are growing as more people live to older age.
While it has long been known that Alzheimer’s involves the death of brain cells, it is still unclear what is going on at the molecular level.
For decades, the prevailing theory was that the cause is build up in the brain of a protein called amyloid.
This led to an army of drugs called antibodies being designed to rid the brain of amyloid. Unfortunately, while many succeeded in wiping out amyloid, they didn’t improve anyone’s Alzheimer’s symptoms.
Finally, two amyloid-busting drugs arrived that do cause a slight slowing in memory deterioration. But Nice, the body that decides whether new medicines can be offered through the NHS in most of the UK, said that their small benefits are not worth the costs and the risk of side effects. The drugs cause brain swelling and bleeding visible on brain scans in up to a third of patients.
I argued here last year that Nice had made the right decision. The latest study has strengthened the case for the NHS ban. It is a review of all the large trials of nine amyloid antibodies – including the two that are available privately in the UK, donanemab and lecanemab – and concludes they are “likely to have no clinically meaningful positive effects”.
Effects too small to be noticeable
In other words, while their effects on slowing memory loss were just about detectable using detailed memory tests in the trials, they were not large enough to be noticeable by patients and their families.
Lilly and Eisai, the manufacturers of the antibodies donanemab and lecanemab, respectively, said that giving an average efficacy for all the amyloid drugs grouped together is invalid.
But the researchers who carried out the study responded that it was valid because they all work broadly the same way.
Plus, the individual efficacy estimates for donanemab and lecanemab are just as small as the result for the whole group, they said. “They are perfectly in line with the pooled estimate,” said Dr Francesco Nonino, a neurologist at IRCCS Institute of Neurological Sciences of Bologna, Italy, who was involved in the study.
The two manufacturers have appealed to Nice to review its decision, but the results of that second review are likely to be at least several months away.
A spokesperson for Lilly said: “We remain steadfast in our confidence in the clinical effectiveness of donanemab.” A spokesperson for Eisai said: “Extensive long-term clinical data show that patients who receive lecanemab continue to benefit from this treatment.”
The treatments that do work
The current focus on amyloid antibodies is distracting families and doctors from existing treatments that do help, said Professor Rob Howard, an old age psychiatrist at University College London.
Two medicines, called donepezil and memantine, are approved by Nice for treating Alzheimer’s. But only about half of people with the disease are offered them, said Howard. “Clinicians aren’t really pushing the established drugs,” he claimed.
This may be partly because, while the amyloid antibodies are said to be “disease modifying” – because they address its root cause – the existing medicines only reduce symptoms by making people a little more alert.
Despite that, the existing medicines’ benefits to memory are about twice that of the amyloid antibodies. They can also be used in combination with each other for a greater effect.
Another barrier is that they can cause side effects, such as nausea and diarrhoea, which may put doctors off from suggesting them, but they are usually minor, said Howard. “We’re a bit timid about starting them and continuing them.”
Other kinds of Alzheimer’s treatments are in development. The largest group of candidates are designed to reduce symptoms, in a similar way to the existing medicines, by stimulating nerve cell activity.
“They help the nerve cells work better, talk better, remember better,” said Professor James Rowe, a neurologist at the University of Cambridge.
Another strategy is to protect nerve cells from dying. “A lot of the new drugs are trying to help cells work better under stress and survive the stress of Alzheimer’s, so they keep working,” said Rowe.
Rival theory to amyloid
A further category involves disease-modifying drugs that work in a different way to targeting amyloid.
The main rival to the amyloid theory of Alzheimer’s is that nerve cells really die because of the build-up of a second protein called tau.
Several drugs that eradicate tau are in development. “I think both amyloid and tau are important,” said Rowe. “Probably to really get on top of Alzheimer’s, you need to treat both in conjunction.”A trial that combines an amyloid antibody along with a tau-targeting drug is currently ongoing in the US.
“It might be that with Alzheimer’s treatments, you want to hit the amyloid and the tau and something else to have triple action,” said Rowe. “We do that with HIV, cancer and heart disease.”
Put like that, the goals of being able to stop Alzheimer’s disease from progressing, or even reversing it, appear some way off. But Rowe is optimistic. “The first HIV drugs, the first clot-busters for heart attacks, were also less effective – yet they were the forerunners of a better future.”
I’ve also written
With the four Artemis II astronauts safely home, here’s what their mission achieved.
I’ve been watching
I grudgingly accompanied my daughter to see the new film, The Drama – which follows a loved-up couple in the days before their wedding. Starring two teen favourites, Robert Pattinson and Zendaya, I was expecting a schmaltzy rom-com, but I was completely wrong.
The interlayering of black humour with a finely judged dissection of Gen Z’s narcissistic tendencies and competitive victimhood made it reminiscent of a Woody Allen movie. It was by turns knowing, gripping, and sometimes gasp-out-loud shocking. It gets five stars from me.
Hence then, the article about these new alzheimer s drugs could transform treatment was published today ( ) and is available on inews ( Middle East ) The editorial team at PressBee has edited and verified it, and it may have been modified, fully republished, or quoted. You can read and follow the updates of this news or article from its original source.
Read More Details
Finally We wish PressBee provided you with enough information of ( These new Alzheimer’s drugs could transform treatment )
Also on site :
- Best-Selling Author’s Novel Named Among ‘Best Books of All Time’
- Target's 'Really Cute' Accent Table Is Giving Massive West Elm Vibes for Way Less
- All of Prince Harry’s Candid Quotes About ‘Messy’ Dad Life During Australian Tour