Seniors Housing & Healthcare Trends

LONDON: Prof Catherine Mummery believes promising new treatments could slow cognitive decline, enhance quality of life and save billions.

As a little girl, Prof Catherine Mummery would wake in the night, convinced the bogeyman was in her bedroom. In fact, it was her grandfather, lost in the house and unable to find his way. He had come to live with the family, although she was too young to understand why. “That was really frightening. I can still vividly remember it,” she says.

She was told his problems were caused by war wounds and shrapnel in his brain. Only much later did she learn that he had Alzheimer’s. “Nobody mentioned Alzheimer’s disease while he was alive. I only found out much later. In those days, it was something you hid under the carpet. You look after the family. You never really get a diagnosis, and you certainly don’t get any help.”

Decades later, her father began to change. A consultant microbiologist, married to a GP, he belonged to a family better equipped than most to recognise disease. His daughter was by then working in dementia.

In his early 70s, he became less organised, more easily agitated, then forgetful. Prof Mummery arranged for him to see a specialist, assuming that the diagnosis would be explained to him. But although he was prescribed medication, he somehow came away without understanding that he had Alzheimer’s.

For all her experience as a dementia specialist, she decided it fell to her to break the news to her father. She arranged a day out together, hoping to soften the blow. But when the moment came, she could not bring herself to tell him. “I bottled it,” she says. Instead, she told him they were simply having a nice lunch.

‘High-risk people could have treatment within five years’

Today, Prof Mummery, professor of neurology at University College London at Queen Square Institute of Neurology and consultant neurologist at University College London Hospital, is helping lead a transformation she hopes will spare another generation those experiences: the fear, the silence and the assumption that nothing can be done.

Her ambition is startling. Within five years, she hopes people at high risk of Alzheimer’s could receive preventive treatment, before symptoms begin. “I would hope that the high-risk people could have treatment within five years.”

This is a conditional hope, dependent on successful trials, regulatory approval and services preparing now. But it rests on research already happening, rather than some distant scientific discovery.

Two major prevention trials, Ahead 3-45 and Trailblazer-ALZ 3, are testing whether drugs can delay or prevent symptoms in people with biological signs of Alzheimer’s who are still cognitively healthy. The studies use lecanemab and donanemab, the first treatments proved to slow decline in people with early symptoms. The former has UK sites, while the latter is being conducted primarily in the US.

Prof Mummery expects results in 2028. “If they’re positive, that changes the world.”

The question is whether treating the disease earlier, while there is more to protect, can keep people well for longer. There is already a tantalising indication that it might.

Research involving families carrying rare genetic mutations that cause Alzheimer’s found that the longest-treated participants who began without symptoms had roughly half the risk of progressing.

The finding came from a small subgroup and was not definitive proof of prevention. But it points towards the possibility of years of additional life without symptoms.

“That could mean five years more… that could mean 15 years more without symptoms. Everybody would say that’s meaningful.” Larger prevention studies are underway to establish whether early intervention can help people without those rare mutations.

“If that confirms it, imagine how the world looks. You’re no longer looking for diagnosis with symptoms for years and giving something to people when it’s quite late down the line. People will want to know whether they’ve got these risks pre-symptomatically or not, and they will want treatment. So we have to change.”

For families accustomed to waiting for deterioration, it would mark a profound shift. Instead of a diagnosis explaining what has already been lost, a test could offer the chance to protect what remains.

‘It makes sense to try to use multiple drugs’

Prof Mummery imagines a screening kit arriving at home, rather like the invitation to bowel cancer screening. A finger-prick test would identify people needing further investigation; doctors could assess their risks and discuss what to do next.

This is her vision, not an available NHS service. But blood tests are already changing Alzheimer’s research and diagnosis, and finger-prick approaches are being studied.

“All of the things I’m talking about are already happening – happening in research,” she says. “That is entirely possible. We did it with cancer.”

Ultimately, she believes many patients will need a cocktail of drugs, tailored to their disease, just as combinations of treatments have transformed cancer and HIV.

Alzheimer’s attacks the brain on several fronts. Amyloid protein begins accumulating years before symptoms appear, while another protein, tau, forms tangles inside nerve cells, disrupting their function. The brain’s immune cells, which normally help clear harmful substances, can become overactive, triggering inflammation that causes further damage. Genes influence how vulnerable people are to these processes.

Tackling just one part of the disease may therefore never be enough. “If you’re going to try to treat a disease that has multiple factors, it makes sense to try to use multiple drugs,” Prof Mummery says. She describes amyloid accumulating for perhaps 20 years before symptoms, until it reaches a point where “it lights a match and the forest fire happens”: tau accelerates through the brain as symptoms develop.

The first amyloid-clearing drugs have demonstrated that the disease can be slowed. They do not cure Alzheimer’s or restore lost abilities. So far, published research suggests that they can reduce decline by around 30 per cent. Unsurprisingly, Prof Mummery wants much more. “We’ve got to get that other 70 per cent, preferably cure it, but we’ve got to get a greater degree of benefit.”

The idea is to clear amyloid, tackle tau and help the immune system protect the brain. Which drugs someone receives could depend on what tests reveal and how far their disease has progressed.

“You will have a combination or a cocktail of therapies that are tailored to what you need at that stage,” she says. “That’s got to be the way forwards. It’s what we do with cancer.”

Gene-silencing treatments could result in fewer hospital visits

Among the most closely watched advances is gene silencing: reducing the production of proteins implicated in Alzheimer’s by interfering with the instructions cells use to make them.

One such drug, diranersen, targets tau. A trial involving 416 people with early Alzheimer’s reduced the protein and produced encouraging results on several measures of cognition and function. The strongest clinical effects were seen with the lowest dose, given every six months into spinal fluid.

There is an important qualification: the trial missed its primary endpoint, which tested the relationship between dose and benefit. A larger trial is planned to establish whether the encouraging findings translate into reliable benefit. Prof Mummery expects UK patients to be recruited when it opens in spring 2027. “There are already patients asking me to go into it.”

Other experimental gene-silencing treatments could require injections only once or twice a year, potentially replacing much more frequent hospital visits. “So you could have an intrathecal injection once a year,” she says, referring to delivery into spinal fluid.

That remains a significant procedure, but very different from frequent hospital infusions.

Researchers are also developing ways to deliver gene-silencing medicines through an ordinary injection under the skin. That requires overcoming one of the brain’s most formidable defences: the barrier that protects it from potentially harmful substances in the blood, but also keeps out many medicines.

So-called brain shuttles exploit the body’s own transport routes to carry drugs from the bloodstream across the blood-brain barrier and into the brain. Trontinemab, an experimental amyloid-clearing treatment, uses this approach.

Researchers are testing whether similar technology can deliver gene-silencing treatments targeting tau. “We can now give gene-silencing therapies as a subcutaneous injection, which completely changes the availability of that drug to people, and that’s being trialled right now.” Prof Mummery shows images from an experiment in monkeys comparing two ways of delivering drugs to the brain.

Injecting treatment into the fluid surrounding the brain and spinal cord produces patchy results, with little reaching deeper structures. But a new technique known as a transferrin receptor brain shuttle, which exploits the system normally used to carry iron into the brain, achieves a much more even spread, reaching areas previously difficult to treat.

It raises a basic question about past disappointments: have some drugs struggled because enough medicine never reached the right place? “They’re not getting there,” she says. “This gets them there.”

Delivery is only part of the answer; trials must still prove that these treatments help patients. But making medicines easier to administer could also make them available to many more people.

The brain’s immune system is another promising target for treatment. Its cells normally help clear debris and abnormal proteins, acting as “cleaning housekeepers”. But an immune response that initially protects the brain can become overactive, causing inflammation and further damage.

“There are some changes that are protective. Then, if it switches into chronic inflammation, it starts to be destructive, and that’s what we think is happening. So it’s really important that we have something that can combat that.”

An experimental oral treatment aims to change that inflammatory response. Because it is a pill, rather than an infusion, it could be taken at home, making treatment potentially far cheaper to roll out, albeit with monitoring scans and checks.

Another approach borrows from cancer treatment, using an experimental drug called IBC-Ab002 to rejuvenate the ageing immune system. It works by releasing the brakes on immune cells, potentially helping the body combat Alzheimer’s without the drug needing to enter the brain.

“You don’t even have to get the drug into the brain. This is what’s so fantastic,” Prof Mummery says.

An early international study involving British researchers found encouraging changes in immune activity and biological markers of Alzheimer’s. It has not established that the treatment slows the disease, but a larger trial is being developed. “Those are very small numbers. It’s just an encouraging signal,” she says.

For all this scientific ingenuity, one of the most immediately useful developments sounds almost mundane: a five-minute MRI. A conventional scan can take half an hour or more. For somebody with cognitive impairment, lying still inside a scanner may be difficult. Movement can spoil the images, while long appointments restrict access.

Prof Mummery describes a pilot involving more than 100 people that tested a streamlined assessment using a short MRI and a blood test, reducing reliance on lengthier and more burdensome investigations. “We showed that it’s as good for diagnosis, and it’s as good for picking up safety issues with the new treatments,” she says. “When you look at the results, they are actually, in some cases, better, not just as good, because people don’t move.”

The approach is being tested across at least 20 UK sites.

‘Political will has to translate into policy’

Shorter scans do not automatically create six times as many appointments: safety checks, changing clothes and moving patients also take time. Her team has examined those processes too. Initially, she hopes services could at least double the number of scans they provide. Without diagnosis and monitoring, drugs cannot reach patients.

But here, her optimism meets a blunt assessment. “The NHS is not ready for these treatments right now.”

Clinicians are trying to improve services, but face limited budgets and competing priorities. Prof Mummery wants political commitments translated into requirements on the NHS organisations funding care. “That political will has to translate into policy, and that has to translate into mandate to change what is happening, because otherwise it will not be seen as a priority in a very hard-pressed NHS.”

She is among 48 leading specialists who this week urged ministers to take action and break the deadlock on access to breakthrough treatments. The call, backed by this newspaper, Lord Cameron and two former health ministers, puts pressure on health secretary Yvette Cooper, who is now understood to be examining the matter, and most crucially on Andy Burnham, who has vowed to make dementia a national priority.

For her, the failure is also moral. Dementia has too often been treated as an unfortunate consequence of ageing, with families expected to absorb the burden.

“For too long, we’ve been accepting that it’s OK for people with a terminal disease to not get a diagnosis and to not have any treatments. That’s not acceptable.”

She wants a movement comparable in ambition to those that changed cancer and HIV care, with clear targets and urgency. “What we need is a recognition that this is urgent, and that tinkering around the edges is not an option.”

The argument over the first amyloid-clearing drugs exposes that gulf. In 2024, the UK became the first country in Europe to license the first drugs found to slow progression of Alzheimer’s. Lecanemab and donanemab were found to slow decline by around one third in patients with early disease. The NHS rationing body, the National Institute for Health and Care Excellence (Nice), judged their benefits insufficient to justify their costs.

But Prof Mummery believes the calculations have failed to capture the true burden of Alzheimer’s on families, and the value of delaying its progression.

Dementia costs the UK an estimated £42bn a year, much of it falling on families through unpaid care, lost earnings and care bills. Yet much of this wider burden falls outside the costs considered in Nice’s assessments.

In its original appraisal, Nice used estimates suggesting that the quality of life of an unpaid carer fell by just 4 per cent between looking after someone with mild cognitive impairment and someone with severe dementia. The figure was widely criticised by dementia experts, who argued that it bore little resemblance to the realities of caring for someone with advanced disease.

Prof Mummery calls the division between health and social care “nonsensical”.

‘We need to have a much better handle on the costs to people’

Someone with mild cognitive impairment might still work, drive, cook and look after grandchildren. Someone with severe dementia may need constant supervision and help with the most basic tasks. She has seen families in which a 19-year-old granddaughter stopped attending university to become a full-time carer. “We really need to have a much better handle on the costs to people and the burden on people, and what these treatments will change on that.”

Her father’s experience remains a reminder of what services get wrong and what that means for families. His treatment for prostate cancer was excellent, she says. But after he broke his hip as a consequence of that treatment, he became confused following the injury and operation.

The acute hospital teams, she says, did not understand his dementia or know how to manage his confusion. She describes their handling of it, and the plans for his discharge, as “absolutely appalling”.

He died aged 78, 10 years ago. Afterwards, Prof Mummery and her mother shared the same thought: “Thank God cancer got him before Alzheimer’s did.” Today she adds: “It sounds awful to say but we still had a lot of him left, which was important.”

But even for a family steeped in medicine, the diagnosis had been difficult to confront.

“Even he and Mum found it difficult to come to terms with the diagnosis,” she says.

Nor did her own expertise make the experience any easier. “I found that the fact that I knew what was happening did not help me very much in how to manage that in the non-professional capacity,” she says. “It is very different being on the other side as a daughter of somebody, seeing how difficult the system is to navigate.”

Her own route into neurology began with a fascination for detective work, the brain and how the mind operates. Before becoming a neurologist, she completed a PhD studying language and semantic processing.

But it was the helplessness she witnessed in families facing dementia that drew her towards clinical trials, offering patients something they could choose to do when so little else was available.

“If you are seeing people in the situation that they’re losing their loved ones and they have nothing that they can do, you want to be able to give them something that makes a difference.”

‘We have an opportunity now that we have a duty to grab’

A survey by the UK Dementia Trials Network and Alzheimer’s Society received more than 1,200 responses from people living with dementia and carers, she says.

More than 90 per cent wanted information about clinical research; fewer than 20 per cent received any. Fewer than 2 per cent had entered a clinical trial.

“It’s not that people don’t want to go into trials. It’s that they’re desperate to go into trials, but they can’t get there. We have to be better at that system.”

The network has developed a Dementia Trials Finder to help. Participation cannot guarantee benefit, but having a choice matters. “It’s also a way of taking back control. Doing something, acting, rather than just this helplessness.” Prof Mummery thinks about her own risk, including whether she carries two copies of a gene variant associated with Alzheimer’s, but has not been tested.

Family history, she stresses, is not destiny. “Just because you have people in your family that have Alzheimer’s disease does not mean you’re going to get Alzheimer’s disease. The biggest risk is still age.” Prof Mummery wants people to understand that, even before preventive medicines become available, there is much they can do to reduce their risk.

Research suggests that around 45 per cent of dementia cases worldwide could potentially be prevented or delayed by addressing 14 modifiable risk factors, including physical inactivity, smoking, excessive alcohol consumption, high blood pressure, obesity, diabetes and hearing loss.

What is good for the heart, she stresses, is generally good for the brain. She distils her advice on building the brain’s resilience into three words: move, eat and think. Raise your heart rate through exercise several times a week; follow a healthy Mediterranean-style diet; and keep mentally active with enjoyable activities that challenge and stretch the brain.

For the little girl frightened by her grandfather’s confusion, and the daughter who struggled to name her father’s illness, the ambition is deeply personal: that future generations will not have to endure the same fear and helplessness.

“I’m hoping that my generation will not have to go through those things that they went through, and that we can change things now,” she says. “We have an opportunity now that we have a duty to grab.”