The first drug shown to slow brain decline in Alzheimer’s disease will no longer be available on the NHS, after a decision was made by the drug’s regulator.

The decision to fund lecanemab has caused dismay and disappointment among people who hoped the drug could help combat a terrible and devastating disease.

But the decision is also not surprising.

Lecanemab is not a “miracle drug”. The European Medicines Agency looked at the same data as the UK and concluded that the drug should not be prescribed to anyone outside a clinical trial.

But what does it take to get an Alzheimer’s drug reimbursed by the NHS?

The National Institute of Health and Care Excellence is tasked with figuring out what is a good use of taxpayers’ money. It is where emotion, desperate need and lobbying for therapies collide with the cold, hard calculations of cost-effectiveness.

In the past, dementia medications have been approved to help manage symptoms such as confusion.

But this is the first time that a disease-modifying drug has been evaluated, a familiar experience in other diseases. Earlier this summer, the cancer drug Enhertu was launched, which could extend the lives of some people with incurable breast cancer. was rejected because it was too expensive.

But even very expensive drugs – I have reported on them one-time gene therapy with an official cost of £2.6 million – could be approved if the benefit is great enough.

Lecanemab has issues with effectiveness, cost and safety.

It was hailed as the first drug to do something, anything, to slow the progression of Alzheimer’s disease. For a field that had suffered repeated failures, this was a truly significant moment when the data came out in 2022. But as I wrote at the timethe effect is small.

Lecanemab does not cure, reverse or stop Alzheimer’s disease. It slows the rate of decline.

In trials, the disease continued to rob people of their brain power, but that decline was slowed by about a quarter over the course of 18 months of treatment. On an 18-point scale ranging from normal to severe dementia, those who got the drug were 0.45 points better off.

How meaningful these effects are is still hotly debated among researchers.

Some argue that they give people longer vital independence. Others argue that the effects are so small that a doctor would not be able to tell the difference between a patient given lecanemab for 18 months and another given a placebo (dummy treatment). Others say that patients should be able to make an informed choice about what is important to them.

The data about the drug came from a large-scale trial with 1,795 volunteers with early-stage Alzheimer’s. But the participants were healthier and younger than people who are normally diagnosed. It raises questions about the “true” effectiveness of the drug in older, frail people with multiple health problems and even “mixed” dementia, which could be part Alzheimer’s and part another disease.

A more powerful drug with a clearer effect on the course of Alzheimer’s disease could break these cost-effectiveness calculations.

That could potentially still be lecanemab. It is possible that starting treatment even earlier in the disease or continuing treatment for longer would have greater effects. This is still unproven.

Or it could be that lecanemab leads the way, and a future drug that follows in its footsteps could provide the greatest benefit. Medical research often needs the first breakthrough that others can build on. The first HIV drugs ultimately paved the way for modern antiretroviral therapy, which gives people a near-normal life expectancy.

Cost is the other side of this equation. A cheaper drug has to do less to meet that value-for-money threshold.

Lecanemab is expensive. The drug itself costs around £20,000 per patient per year (based on US prices). But the care around it doubles that cost on the NHS (and private rates are likely to be even higher).

Before treatment can begin, an expensive PET scan (positron emission tomography) or lumbar puncture is needed to collect cerebrospinal fluid and determine whether the patient actually has Alzheimer’s. There are many different forms of dementia.

Then, every two weeks, an infusion into a vein is needed to administer the drug, and expensive brain scans are needed to monitor the known side effects.

One option is to negotiate a better price. With other drugs on the way, like donanemab, there will be competition that could bring prices down.

There is still time for this to happen. NICE published its draft decision on Thursday, which will be finalised later this year.

Pharmaceutical companies, however, want to recoup the costs of their years of research and development. But the field has produced many expensive failures and dead ends.

Both lecanemab and donanemab are also a very expensive type of medicine called monoclonal antibodies. These are lab-made versions of the antibodies that your immune system makes naturally to fight disease.

For Alzheimer’s, they’re designed to target a sticky protein called amyloid that clogs the gaps between brain cells. Amyloid is a hallmark of Alzheimer’s, and the antibodies remove it.

However, these are difficult to design and produce, which inevitably makes them expensive drugs. You can’t get monoclonal antibodies for aspirin prices.

The drug also should not be used in people with certain genetic mutations that actually have a higher risk of Alzheimer’s. In that case, a genetic test is required.

Dangers of these drugs include brain swelling and brain bleeding or hemorrhaging, and some have been fatal. So monitoring increases the cost.

Blood tests to diagnose Alzheimer’s, drugs that require fewer infusions or cause fewer side effects, or better ways to predict who is at risk of side effects could also theoretically reduce the costs of care surrounding these drugs.

But as things stand, treating the 70,000 people who would technically qualify for the drug in England could cost around £1.4 billion a year, and a similar amount in NHS care. That has been judged a poor use of taxpayers’ money for a drug with an impact widely regarded as “small”.

It is still a historic week. For the first time, a drug has been approved that can slow the pace of Alzheimer’s disease.

For decades, dementia was seen as an inevitable part of aging, then it became clear that it was actually a disease. Now there is optimism that we are on the verge of doing something about it.