SCIENTISTS have hailed "hugely exciting" results from a large clinical trial which found that an experimental Alzheimer's drug slowed cognitive decline by around a third compared to a placebo.

The medication, donanemab, has raised hopes that patients could soon have access to a second effective treatment for the brain-wasting disease following a previous approval for lecanemab.

Both are anti-amyloid drugs, which work with the body's immune system to attack and clear protein plaques from the brain in patients with early-stage disease.

The US pharmaceutical firm behind donanemab, Eli Lilly & Co, said it will now lodge an application for approval from the US Food and Drug Administration by the end of June.

It comes after the FDA granted accelerated approval for lecanemab in January this year following clinical trials showing that it slowed cognitive decline by 27% over 18 months.

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The drug is not yet available in the UK and clinicians and charities have raised concerns that the NHS is not set up to diagnose Alzheimer's at an early enough stage, when anti-amyloid medications can be prescribed.

The Phase Three clinical trial of donanemab compared outcomes in more than 1,700 participants over 18 months.

Patients were split into two groups based on the levels of tau - a type of protein tangle - present in MRI scans of their brains.

These are believed to be triggered into forming in clumps around neurons as a knock-on effect from the initial build up of amyloid plaques.

Patients with larger tau build ups are at a more advanced stage of the disease.

According to results posted by Lilly - which are yet to be peer-reviewed - patients with earlier-stage disease who received a monthly infusion of donanemab experienced a 35% slower decline than comparable patients on a placebo drug, based on protein deposits in brain scans.

Overall - across patients at all tau levels - the slowdown averaged 22%.


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A majority of patients receiving donanemab – 52% – were able to stop taking the medicine by one year, and 72% were able to do so by a year and a half due to positive effects on functions such as thinking, language and memory.

The findings reinforce the importance of administering the medication at an early stage, when symptoms may be very mild.

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Lilly’s chief scientific and medical officer, Dr Daniel Skovronsky, said this was “the kind of efficacy that’s never been seen before in Alzheimer’s disease".

Side effects were reported including three deaths among trial participants on the drug which have been attributed to brain swelling or microhemorrhages, known as amyloid-related imaging abnormalities or ARIA. Similar rare events were also reported for lecanemab.

Overall, brain swelling occurred in 24% of the participants, with 6.1% experiencing symptoms, while brain bleeding occurred in 31% of the donanemab group versus 14% of the placebo group.

John Hardy, a professor of neuroscience and a group leader at the UK Dementia Research Institute at University College London (UCL), said having two drugs would be "great for competition", adding: “There is much work still to do if these drugs are approved as they should be.

"From a practical perspective we need to organise how to get these drugs into patients safely, and from a research perspective we need to understand why they slow disease but do not – yet at least - seem to stop progression.”

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Dr Charles Marshall, a clinical senior lecturer and honorary consultant neurologist at Queen Mary University of London (QMUL), said: “This is hugely exciting news, as it provides further evidence that it is possible to slow down Alzheimer’s disease.

"When the full results are published as a paper we will be able to start carefully balancing the risks and benefits, and this will inform decisions about whether donanemab should be routinely given to patients with Alzheimer’s disease.”

Dr Richard Oakley, associate director of research at Alzheimer’s Society, said: “After 20 years with no new Alzheimer's drugs, we now have two potential new drugs in just twelve months – and for the first time, drugs that seem to slow the progression of disease.

"This could be the beginning of the end of Alzheimer’s disease."

Dr Marc Busche, also a group leader for the UK Dementia Research Institute at UCL, said the trial was a "real breakthrough". 

He added: "Notably, the beneficial effect was smaller in those with high tau levels, suggesting a potential interaction between these pathogenic proteins.

"Looking ahead, I anticipate that concurrently targeting amyloid-beta and tau could lead to even better patient outcomes, making this a crucial focus for future research and the next generation of clinical trials.”