Solanezumab blocks memory loss in patients with mild version of the disease, making it the first medicine ever to slow pace of damage to patients’ brains

Scientists appear to have broken a decades-long deadlock in the battle against Alzheimer’s disease after announcing trial results for the first drug that appears to slow the pace of mental decline.

The drug, called solanezumab, was shown to stave off memory loss in patients with mild Alzheimer’s over the course of several years. The effects would have been barely discernible to patients or their families, scientists said, and it is no cure. But the wider implications of the results have been hailed as “hugely significant” because it is the first time any medicine has slowed the rate at which the disease damages the brain.

“This is the first evidence of something genuinely modifying the disease process,” said Dr Eric Karran, director of research at Alzheimer’s Research UK. “It’s a breakthrough in my mind. The history of medicine suggests that once you get through that door you can explore further therapeutic opportunities much more aggressively. It makes us less helpless.”

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Existing drugs help with the symptoms but ultimately do nothing to slow the disease’s progression.

The drug, developed by the American company Eli Lilly, had previously been tested in a larger group of patients with both mild and moderate dementia and this trial had appeared to end in failure in 2012.

However, when scientists analysed the data more closely, they found that in the 1,300 patients with mild dementia, those who had been placed on the drug showed a roughly 30% slower decline in memory and cognitive tests than those who had taken a placebo during the 18-month trial.

This was a fairly small difference from the perspective of the patients who had not yet suffered the devastating memory loss or profound changes to personality that come later on. But the result hinted that the drug could work as long as it was given early enough.

Questions remained about whether the drug was simply treating the symptoms – improving a patient’s mood or concentration – rather than actually delaying the loss of neurons in the brain, which drives memory loss.

To test this, Eli Lilly switched the half of the 1,300 patients who had been on the placebo on to the drug as well and the entire group was given solanezumab for a further two years.

If the drug was just treating the symptoms, the placebo group would be expected to “catch up” over time. However, the results, unveiled on Wednesday at the Alzheimer’s Association International Conference in Washington DC, in the US, showed that the differences between the two groups were still there – a sign that the drug had made a genuine impact on the progression of the disease.

“It deflected the course of the disease in an irrevocable manner,” said Karran, who previously worked for Eli Lilly.

The company is now looking to see whether the drug is more effective when given at an earlier stage – something that might be expected given that it apparently had no effect for patients with more serious dementia. “It’s entirely possible you’ll show an even bigger benefit if people are given solanezumab earlier on,” said Karran.

Scientists said the results also support the idea that sticky plaques in the brain – the most visible hallmark of the disease – are what causes mental decline. The drug is an antibody that works by disassembling the building blocks that make up the plaques, slowly causing them to disintegrate.

Until now, drugs that targeted the plaques have not appeared to have any effect leading some to question whether some other biological process in Alzheimer’s was the real root of the disease.

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Dr Doug Brown, head of research at the Alzheimer’s Society, said: “Today’s findings strongly suggest that targeting people in the earliest stages of Alzheimer’s disease with these antibody treatments is the best way to slow or stop Alzheimer’s disease. These drugs are able to reduce the sticky plaques of amyloid that build up in the brain, and now we have seen the first hints that doing this early enough may slow disease progression.”

The positive trial results follow years of failed clinical research. Between 2002 and 2012, 99.6% of drugs studies aimed at preventing, curing or improving Alzheimer’s symptoms were either halted or discontinued at huge financial cost to drugs companies, many of whom shut down dementia programmes as a result.

Richard Morris, professor of neuroscience at the University of Edinburgh, said the result was likely to be significant – although he added that he was reserving final judgment until he saw the data in more detail. “I am cautiously optimistic, from the perspective of the audience, they should be too,” he said. “This is not a mouse study, it’s a people study. And that matters.”

Even if further trial results are positive, it is likely to be several years before the drug would become available on the NHS. Another phase-three trial is due to report in 2016 and then the drug would need to go through regulatory approval and would need to be shown to be sufficiently beneficial to patients.

About 225,000 people will develop dementia in the UK this year – a rate of one every three minutes.

Alzheimer’s Society research shows that 850,000 people in the UK have a form of dementia, and that in less than 10 years, 1 million people will be living with dementia. This is expected to rise to 2 million by 2051 unless preventative treatments are developed.