Alzheimer’s breakthrough

The discovery of the first ever drug to slow down memory loss associated with Alzheimer’s has been hailed by scientists around the globe as a groundbreaking moment in the struggle to treat the disease.

The drug in question is Lecanemab, an antibody therapy which removes clumps of protein which build up in the brain. While no cure, a clinical trial on almost 18000 patients has confirmed that it slows down cognitive decline in patients with early stages of the disease. Developers of the drug are Biogen in the US and Eisai in Japan, who first announced the results of their clinical trials in September, and have just published the full data. 

The news has attracted vast attention as Alzheimer’s affects 30 million people worldwide and accounts for nearly two-thirds of dementia cases. It is the leading cause of death in the UK and almost a million Brits suffer from this form of dementia. 

There are, however, some fairly major caveats. The effect of the drug is somewhat modest: It reduced the decline in patients’ overall mental abilities by 27% over 18 months. While optimistic doctors believe this reduction could give patients months more of independent living, others are sceptical that the difference would be this quantifiable. 

Lecanemab carries a high price tag too. The antibodies are expensive to produce in the lab meaning the treatment could cost between £10,000 and £30,000 per patient a year. Given the modest improvements, drug regulators may still decide that it is not cost-effective. 

If Lecanemab does manage to gain regulatory approval in the new year, scientists are hoping that it could be available on the NHS from September. Yet big hurdles remain when it comes to rolling out the treatment widely. 

Crucially, the NHS lacks sufficient diagnostic tests to identify those most likely to benefit from the drug. There is also doubt as to whether it is equipped to provide the multiple MRI scans required throughout treatment to monitor potential side-effects, such as brain swelling and haemorrhages.

And then there is the issue of actually administering the drug: Lecanemab cannot be taken as a tablet at home. Rather, patients would need to come into hospital every two weeks to receive an infusion of the drug, absorbing precious resources in the already overstretched and understaffed health service. 

All in all, Lecanemab is far from a magic cure, and there are major hurdles to overcome if it is to be administered widely. 

But does this mean that today’s discovery – or so-called “breakthrough” – has been overegged? 

Arguably not, when we remember that, for decades, scientists’ ardent attempts to identify any effective treatment to slow, halt or reverse the disease have been outright failures.

After years of setbacks, today marks tangible progress. And it offers hope. 

Indeed, as Jonathan Schott, professor of neurology at UCL and chief medical officer at Alzheimer’s Research UK, puts it: “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.”

That in itself is a big breakthrough. 

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