We almost missed the first warning signs my husband, 56, had dementia. Then we found a drug that SLOWED his decline and allowed us to just get on with life again… so why are we having to pay £80,000 a year?

Talking about an old company logo was the first real sign things were not quite right with Nick Brake.

On a trip to Norfolk in 2020, his wife, Nicky, commented that the ruins of a medieval church reminded her of the branding of the furniture business Nick had run for 15 years – a simple line-drawing of a Gothic archway. Yet Nick, then 56, couldn’t picture it at all.

‘He’d always been very sharp and switched on,’ says Nicky, 59. But the episode made her reconsider some other changes she had noticed.

Nick, always a good speller, had begun asking her how to spell words. He forgot things that happened the day before. In conversation, he struggled to find words – and Nicky found herself filling them in.

Fast-forward four years, and – despite initially being reassured by their GP that it was nothing – the couple, from Braunston in Rutland, found themselves in front of a consultant neurologist.

‘I might be wrong,’ he told them, ‘but I’m pretty sure you have dementia’.

Blood and urine tests and brain scans confirmed the diagnosis: Nick had young-onset Alzheimer’s disease (when the condition develops in someone under 65). He is one of more than 70,000 Britons said to be living with the condition.

‘It came as a big shock,’ says Nick. ‘After four years of being told I was fine, I’d started to think I was fine.’

For most people with Alzheimer’s, the NHS offers drugs that ease symptoms. The most common, such as donepezil (brand name Aricept) and rivastigmine (Exelon), are cholinesterase inhibitors – developed in the 1990s, these boost levels of a chemical that helps nerve cells communicate, and can help memory and thinking for a time. But they don’t directly treat the damage to the brain.

Nick was prescribed donepezil, but couldn’t have the highest, most effective dose as the drug can slow the heart – and, as a lifelong runner, Nick’s resting heart rate is already low.

Determined to throw everything they could at Nick’s diagnosis, the couple decided to pay for a new Alzheimer’s drug not yet offered on the NHS.

Lecanemab (brand name Leqembi) has made headlines around the world as the first drug to slowdown Alzheimer’s. It’s an antibody treatment that helps the brain’s immune system clear amyloid, a sticky protein that builds up in the brain and is linked to the disease.

In August 2024, just weeks before Nick’s diagnosis, lecanemab was approved by the Medicines and Healthcare products Regulatory Agency.

But it’s been rejected by the National Institute for Health and Care Excellence (NICE), along with a similar drug, donanemab, for the NHS, saying the benefits were too small to justify the cost.

However, for Nick it was ‘a no-brainer’ to pay for it privately.

‘It’s such a massive psychological boost to actually be doing something,’ he says.

‘Before that, we felt powerless. We feel fortunate to be able to pay, but guilty that not everyone can. It should be available to all.’

The drug, which is administered via a drip, can only be given in the early stages of the disease.

In January 2025, Nick saw consultant neurologist Dr Richard Perry, at the Cleveland Clinic in London.

A genetic test showed he carries no copies of APOE4, a gene variant that raises the risk of Alzheimer’s (and the risk of the drug’s most serious side-effects: brain swelling and bleeding). People with two copies are not allowed the drug in the UK.

Nick’s first infusion, a month later, did not go smoothly, drastically affecting his temperature. ‘I was frozen,’ says Nick. ‘It was horrendous.’

About one in four people in the main lecanemab trial, published in 2022, had a reaction like this.

It is due to how the immune system responds to the antibody, causing chills, fever and aches.

It took around 36 hours for Nick to warm up. (Ever since, he’s been given paracetamol and an antihistamine before infusions and had no further problems.)

For the first 18 months Nick had an hour-long infusion every two weeks. Since August, he’s been having one a month.

‘I feel great afterwards,’ he says, ‘and just get on with my life.’

Nick believes the drug is holding him steadier.

Today, he still runs, plays tennis and walks the family’s golden retriever for around two hours every day (the couple are both retired, having run a charcuterie business before closing it during Covid). He also plays jazz guitar.

‘My Alzheimer’s is getting worse, but it’s a much slower decline,’ says Nick.

‘I’m still driving, which I wouldn’t have expected.’ He drives himself to the station and travels to London for his infusions alone.

But he’s honest about what he’s lost. He can’t remember the names of friends and struggles to follow conversations.

Things are hard, but the couple are convinced they’d be harder without lecanemab.

‘It has kept Nick’s quality of life significantly better for longer, which is good for him and so good for all of us,’ says Nicky.

Earlier this year a PET scan – which use a mildly radioactive dye that sticks to amyloid, which is measured in centiloids – put Nick’s amyloid level at 22 centiloids: doctors estimate that previously it had been around 90.

‘This reduction indicates that lecanemab has done the job it is designed to do,’ says Dr Sebastian Walsh, a clinical lecturer in public health medicine at Queen Mary University of London.

‘It triggers the brain’s immune system to remove certain types of amyloid protein which we think are harmful to brain cells.

‘The question is the extent to which this leads to a meaningful change in the experience of Alzheimer’s for a person.’

Nobody can say how fast Nick, now 61, would have declined without the drug. But Rob Howard, a professor of old-age psychiatry at University College London, says his experience is just what the clinical trials predict.

‘What has happened to Nick is exactly what I would have expected,’ he says.

‘The drug has removed amyloid from his brain, but he’s continued to deteriorate.

‘That’s fine if he was only expecting a modest change and understood that he’d continue to deteriorate. It isn’t fine if he expected to see a significant improvement or delay in progression of his symptoms.’

The results of the main trial of lecanemab, published in 2022, found that, over 18 months, patients with early Alzheimer’s taking the drug worsened by an average of 1.21 points on a symptoms scale that runs from 0 to 18 – this compared with 1.66 for those on a placebo. That 0.45-point gap is where the often-quoted ‘27 per cent slowing in disease progression’ comes from.

But doctors usually need to see a change of at least one whole point before they notice a difference in a patient, says Dr Walsh.

‘So the effects of the drug would need to double for us to reliably notice it.’

‘Everyone in those trials continued to deteriorate, whether they received lecanemab or a placebo,’ says Professor Howard, who believes some of the coverage of drugs such as lecanemab has given people ‘unrealistic expectations’.

There are risks, too. In the trial around one in eight developed swelling in the brain – accordingly, anyone taking the drug needs regular MRI scans. Then there is the cost. While Nick and Nicky prefer not to say what they pay, Professor Howard says in the UK it costs around £80,000 a year for treatment.

With all of this in mind, it’s no surprise that NICE rejected the drug, says Professor Howard.

There’s also a wider debate about whether amyloid is the right target at all.

Even drugs that clear large amounts of it bring only small benefits – and some researchers believe another protein, tau, is more closely linked to symptoms.

Others argue the real culprit lies in the brain’s own immune cells, called microglia, as Good Health reported recently.

Supporters of the drug argue that keeping people independent for longer saves money on care.

NICE’s final decision has been paused while the drug companies negotiate a price – an announcement is expected next month.

For the Brakes, there’s solace in feeling they’re doing all they can.

Nick has given up alcohol and now eats three proper meals a day – ‘I used to live off apples,’ he says. He takes supplements including creatine, magnesium and B vitamins and does brain-training activities every morning.

Earlier this month he ran the Oxford Half Marathon, with a group including his son, Stanley, 23, raising money for Alzheimer’s Research UK. ‘It’s so uplifting,’ says Nick.

This summer his daughter, Patsy, 25, took him trekking in the Dolomites in Italy, and he went to Naples with Stanley to watch Chelsea play.

The Brakes are now in the middle of moving house, downsizing to make life easier in the years ahead.

‘We’re doing what we can while we can,’ says Nick.

‘The treatment is buying us time. Time together with

Nicky, time as a family – and time for more treatments to become available.’

alzheimersresearchuk.org