- Scientists expected solanezumab to be the first drug to slow dementia
- Previous trials suggested it stopped toxic plaques forming in the brain
- But US pharma giant Eli Lilly and Company reported it showed no benefits
- It said it was now abandoning plans to apply for a licence for the drug
Hopes of the first effective drug for Alzheimer’s were dashed yesterday, after long-awaited clinical trials showed it did not work.
Scientists widely expected solanezumab to become the first drug to slow down the course of Alzheimer’s disease, the most common form of dementia.
The results are a major setback for dementia researchers, with ramifications for the entire theory of how Alzheimer’s works.
Some warned that investment in research may fall as a result of the blow – which would seriously damage the Government’s pledge to deliver an effective dementia treatment by 2025.
Scientists widely expected solanezumab to become the first drug to slow down the course of Alzheimer’s disease, the most common form of dementia (stock)
Experts have been tweaking and testing solanezumab for more than 15 years, after it was shown to clear the toxic amyloid proteins that form plaques and clumps in the brain.
But yesterday US pharma giant Eli Lilly and Company announced a trial of 2,000 people had shown solanezumab showed no benefit for people with mild Alzheimer’s.
The company, whose share price tumbled following the announcement, said it was abandoning plans to apply for a drugs licence for solanezumab.
Until yesterday morning, it had hoped to roll the drug out for patients by 2018 – and expected to gain £4billion of sales every year as a result.
Dr John Lechleiter, CEO of Eli Lilly, said: ‘The results of the solanezumab trial were not what we had hoped for and we are disappointed for the millions of people waiting for a potential disease-modifying treatment for Alzheimer’s disease.
‘We will evaluate the impact of these results on the development plans for solanezumab and our other Alzheimer’s pipeline assets.’
But yesterday US pharma giant Eli Lilly and Company announced a trial of 2,000 people had shown solanezumab had no benefit for people with mild Alzheimer’s
Dr Mike Hutton, chief scientific officer of Eli Lilly’s neurodegenerative diseases team in Surrey, said the company may pursue trials in patients at a much earlier stage – years before symptoms appear – in case giving it sooner has an effect.
But he added: ‘We have abandoned the idea of using this for patients who already have mild Alzheimer’s.’
Existing drugs for dementia simply address the symptoms without tackling the underlying causes.
But an earlier trial of solanezumab, published last year, raised hopes it might be the first drug to tackle the cause of the disease, meaning it might be able to slow down the course of the disease as well.
Scientists though it did that by clearing away sticky amyloid molecules in the brain – the proteins thought to cause Alzheimer’s – before they group into plaques.
Critics last night said the failure of solanezumab to have a real clinical effect – coming on the back of other high-profile failures – suggested the entire amyloid theory might be flawed.
Professor Peter Roberts of the University of Bristol, said: ‘There is still no convincing evidence that shows a clear relationship between amyloid deposition and deficits in cognition in humans.
‘All we really know is that evidence of amyloid deposition begins up to maybe 20 years before the onset of Alzheimer’s disease. ‘This might be a good indicator, but does not prove causality.’
But Dr David Reynolds, chief scientific officer at Alzheimer’s Research UK, said other approaches might yet bear fruit.
‘Our 15-year wait for a new Alzheimer’s drug does not end today, but we shouldn’t view this setback as the end of the line – the journey towards a new treatment can and will continue.
Experts have been tweaking and testing the drug for more than 15 years, after it was shown to clear the toxic amyloid proteins that form plaques and clumps in the brain
‘It’s very disappointing that solanezumab has not shown benefit for people with mild Alzheimer’s and will no doubt trigger important debate within the research community.
‘There are several other anti-amyloid drugs still in clinical trials that work in different ways, some of which are being tested even earlier in the disease process than solanezumab.’
An estimated 850,000 people in the UK are thought to be living with dementia, with figures expected to rise to one million by 2025, and two million by 2050.
WHAT TO EAT TO PREVENT DEMENTIA
Eating carrots, kale and sweet potatoes could prevent dementia in older adults, research earlier this week suggested.
Consuming the compounds that give plants and vegetables their vibrant colours can bolster brain functioning in older adults.
Those who had lower levels of carotenoids in their system had to rely on more brain power to complete memory-orientated tasks, US scientists found.
The powerful compounds can be found in a range of colourful vegetables and are known to improve cognitive ability.
The Alzheimer’s form of the disease affects 500,000.
Last week the Office for National Statistics announced dementia had become the biggest cause of death in England and Wales, overtaking heart disease for the first time.
Jeremy Hughes, chief executive of the Alzheimer’s Society, said: ‘After positive news last summer we had high hopes for this drug to become the first to slow down Alzheimer’s disease.
‘It’s extremely disappointing to learn that it hasn’t delivered a meaningful change for people living with dementia, when the need is clearly so great.
‘Dementia is society’s biggest health challenge – and we’ve seen time and again that developing effective treatments is incredibly difficult.
‘This is only one drug of several in the pipeline and they aim to tackle dementia in different ways, so we should not lose hope. Dementia can and will be beaten.
‘There will be concern that investment in dementia research may drop as a result of another failure – neither families nor the NHS can afford for this to happen. We must and will redouble our efforts and investment into dementia research.’
Professor John Hardy of University College London said the focus would now shift to another class of experimental drugs called BACE inhibitors, which tackle the production of amyloid at an earlier stage.