The beginning of the end?

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You can take the headline like the one you see above in one of two ways: morbidly, you can be like me, in my mid-50s, wondering whether blanking the name of someone you haven’t heard of or thought about for a while is the warning sign of a bleak future already at a relatively young age. The other interpretation is that it echoes the comment yesterday of experts in the field ofAlzheimer’s research after the breakthrough of a drug, lecanemab, that has been found, for the first time, to slow the disease’s advance.

Although the drug is not a cure, it gives hope to millions of people in the early stages of Alzheimer’s progression - or those at risk - that quality of life should not decline as fast as it does now as the disease wreaks its havoc on the brain. Trials of the drug - delivered intravenously every fortnight - have demonstrated that memory decline can be slowed down by 27% over a period of a year-and-half. No wonder it has the medical world excited, and not in a way seen in more than 30 years of research into the dementia-causing condition which, since 2013, has surpassed heart disease as the second most common cause of premature death after cancer. 

Dementia has long been regarded - even dismissed - as the price of an ageing population, but it's a myth that Alzheimer’s only affects the elderly. A Dutch study found that so-called ‘young onset’ Alzheimer’s came occur in people in their 30s and 40s. Worldwide, it said, as many as 3.9 million people under 65 may be affected. It touches so many lives: my father died with it at the age of 90, a sobering thought for my own destiny. By 2040 it’s expected that 1.6 million people in the UK will have some form of dementia, with Alzheimer’s the leading cause, accounting for 60% of all cases in the UK. No wonder there is such buzz over lecanemab, though it’s not yet clear what impact the drug will have on the-near £35 billion cost of total care that dementia costs the UK. The point here, though, is that a condition previously thought untreatable now is, to a degree. And it gives further hope of preventative treatments for those at risk. 

Now, here are words that I never thought I’d commit to a keyboard, but former prime minister David Cameron made an excellent point when he told the BBC’s Newscast: “Imagine if you could wake up in the morning and simply take a pill that prevents the build up of proteins that cause Alzheimer’s, in much the same way as millions of people take statins to lower their cholesterol and prevent heart disease.” I’m no expert, clearly, but Dave has a point. He also has a personal connection to Alzheimer’s, having lost his mother to the condition, and being the president of Alzheimer’s Research UK charity.

While the excitement today is over lecanemab’s potential for mitigating Alzheimer’s symptoms, not far behind is the prospect of a cure. It is - to be clear - a long way off, but scientists not normally know for their ebullience have hailed the lecanemab breakthrough as the “beginning of the end” of Alzheimer’s, paving the way for treatments that could lead to an eventual cure. 

Some expectation management is, however, required: it has taken more than 30 years to reach this point, ever since UCL professor Sir John Hardy identified a protein called amyloid that causes a form of ‘congestion’ in the brains of Alzheimer’s sufferers. His discovery led to the medical industry pouring millions into drug research to target the protein. Lecanemab is one result of that research, and is a type of antibody that replicates the immune system to remove the sticky amyloid protein that attaches itself to neurons in the brain, progressively inhibiting the organ itself. Further more, the lecanemab could lead to further breakthroughs in research programmes into other drugs and bespoke treatments.

Indeed, Hardy himself has hailed the lecanemab success: “I truly believe it represents the beginning of the end,” he said, reflecting on the three decades since his own discovery. “We now know exactly what we need to do to develop effective drugs. It’s exciting to think that future work will build on this, and we will soon have life-changing treatments to tackle this disease.”

The last statement should not be disregarded, either, as hyperbole. “Once you’re diagnosed, the GP just says there’s nothing that can be done,” Cheryl Essam told the Daily Telegraph today about her husband David’s experience. 78-year-old David joined the lecanemab trial three years ago, receiving treatments every two weeks, but not knowing whether he was receiving the actual drug or a placebo. “People have been looking for hope for 30 years,” Cheryl said. “We weren’t really expecting a positive outcome.” Now, she says lecanemab represents “a light of hope”. 

Sir John Hardy

On Tuesday this week Hardy presented the trial results at an Alzheimer’s conference in San Francisco, revealing that over the years of research, voices in the medical profession suggested that he should have devoted his efforts to other more critical priorities. “I can understand that,” he explained to the Telegraph. ”It’s taken a long time. It’s been a difficult problem and some people have thought that we should have been doing other things.” Now, he says, “I do have a sense of vindication for sure”.

So what happens next? Hardy hopes that people in their 50s and 60s will be able to ask their GPs for an amyloid test which, echoing Cameron’s statin remarks, would be as easily administered as a cholesterol check. Before then, though, lecanemab needs regulatory approval and then adopted for use at scale by the NHS - not as easy as it sounds given the cost pressures the health service is under. Dementia today is chronically under-supported until often it’s too late, and sufferers are forced to sell their homes to pay for round-the-clock care, once it becomes too much for loved ones to take care themselves.

“We have to do better with diagnosis,” Sharon Brennan of the Alzheimer’s Society told the Telegraph, pointing out that symptoms don’t always present themselves until a sufferer turns up at an A&E department confused, in a distressed state, or the victim of an accident caused by the undiagnosed condition. A further complication is that Alzheimer’s is not easily diagnosed, and even when it is, the lack of effective treatment means that doctors and patients alike are reluctant to do anything more than let it progress until the ultimate decline. Thus, the lecanemab breakthrough should not be underestimated.

While no one is getting carried away, the uncharacteristic excitement the drug has generated amongst usually quite stoic scientists has generated hope that there will be a newfound enthusiasm by everyone to press on with developing effective treatments. And, yes, why not a cure. If a vaccine for Covid-19 can be developed in record time with the right momentum behind it, why not an equivalent vaccine for a disease that robs millions of their lives, at a cruelly debilitating pace? Now that would be a breakthrough.