Lecanemab: New Alzheimer’s drug slows memory decline – fueling hope doctors will one day cure dementia | Scientific and technical news

Doctors have hailed a “new era” in medicine after a study showed for the first time that a drug can slow the debilitating symptoms of Alzheimer’s disease.

Results from the clinical trial also revealed that the drug lecanemab cleared clumps of a protein called amyloid – thought to be one of the main causes of the most common form of dementia – from patients’ brains.

The data, released at a conference in San Francisco, sparked an outpouring of optimism from scientists, many of whom had spent decades trying to understand what leads to the disease and finding a cure.

Rob Howard, professor of old age psychiatry at University College London, said the results were “wonderful and hopeful” – adding: “At last we have gained ground on this most dreadful disease and the most dreaded and years of research and investment have finally paid off.

“It feels momentous and historic. It will encourage genuine optimism that dementia can be defeated and even one day cured.”

The drug’s makers released the first results in a press release in early fall, but many doctors held back from celebrating until the full results were released at the clinical trial conference. Alzheimer’s disease.

They showed that lecanemab slowed the decline in memory and mental agility by 27% in patients with mild Alzheimer’s.

“Doctors are optimistic”

Critically, the drug removed so much of the amyloid protein that patients would not have had enough evidence of Alzheimer’s disease on their brain scans to qualify to participate in the trial.

The study strongly suggests that the drug only begins to have a clinical effect once amyloid is reduced to low levels in the brain.

Results after 12 months of treatment suggested it was ineffective – but after 18 months the effect was significant.

Doctors are optimistic that continuing treatment will lead to even better results.

Professor Nick Fox, Director of the Dementia Research Center at University College London, said: “This confirms a new era of modification in Alzheimer’s disease, an era that comes after more than 20 years of work dogged by many, many people, with many disappointments along the way.”

Lecanemab is not a cure. But even slowing the progression of Alzheimer’s disease would be a game-changer, delaying the need for specialist care and allowing people to spend more time with their families.

However, the drug has side effects.

One in eight patients given lecanemab experienced brain swelling and other changes, possibly as a result of amyloid protein removal. But most only had evidence of problems on brain scans. Less than one in 30 had actual symptoms such as headaches or confusion.

Some patients had bleeding in the brain, although deaths were no higher in those receiving treatment than in those receiving a dummy drug.

Nevertheless, this highlights the need for careful monitoring of people on treatment.

Prof Fox said: “Any risk is clearly significant, but I think many of my patients would be very willing to take such a risk.


‘Massive challenge for the NHS’

Doctors have warned that lecanemab will be a huge challenge for the NHS, not just because the drug is given by intravenous infusion every two weeks.

Most Alzheimer’s disease patients are currently diagnosed when they have mild symptoms – too late for treatment with lecanemab. And only 1% have their diagnosis confirmed by a brain scan or lumbar puncture, a biopsy of their cerebrospinal fluid.

Susan Kohlhaas, research director at Alzheimer’s Research UK, said: “It is safe to say that the NHS is not ready for a new era of dementia treatment.

“We estimate that unless there are drastic changes in how people access specialist diagnostic tests for Alzheimer’s disease, only 2% of people who are eligible for drugs like lecanemab will be able to do so. to access.”

Until now, only drugs have treated the symptoms rather than the underlying cause. But if lecanemab is cleared for use by the NHS, delays in treatment will lead to brain cell death and disease progression.

Professor John Hardy, from the UK Dementia Research Institute in London, said the drug was a long time coming.

He added: “I truly believe this represents the beginning of the end.

“The first step is the hardest, and 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’ll soon have treatments that will change the life to fight this disease.”

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