Are scientists finally on the verge of beating DEMENTIA?

An exciting new drug. A revolutionary use of ultrasound. Even injections of young people’s blood. After years of setbacks ...

Deep within the Andes in a coastal town called Yarumal, 5,000 people are at risk of developing Alzheimer’s by their 40s. The locals say they are cursed with La Bobera, or ‘the foolishness’ — a spell that causes people to lose their minds.

But in truth they possess a genetic mutation that causes early-onset Alzheimer’s.

This high chance of developing the disease means scientists can justify testing experimental medicines with the hope that this will lead to new drugs.

Dementia affects 850,000 people in the UK, and this number is set to rise to 1million within the next decade. Around half a million suffer from the most common form, Alzheimer’s — a disease with no cure.

part of the difficulty in finding a cure is that we don’t catch it early enough, says Gordon Wilcock, an emeritus professor of geratology at the University of Oxford. By the time symptoms begin, the brain has already suffered a lot of damage, so drugs have little effect, he adds.

Crucially, the other problem is that we still don’t understand what causes Alzheimer’s. Although amyloid plaques — sticky buildups in the brain — seem to play a role, there are clearly many other factors.

‘It might not even be one disease,’ says professor Wilcock. He says that the Alzheimer’s brain may be an end point that people come to via different paths, meaning there may never be a onesize-fits-all drug.

Despite many promising animal studies, no drug has managed to halt the disease in humans. earlier this year, pharmaceutical giant Merck halted a trial of one of the most promising drugs — verubecestat — after an external board determined there was virtually no chance of it working.

This came just months after another amyloid-busting drug, solanezumab, was abandoned after poor results.

After 20 years of failed drug trials, you would be forgiven for thinking it’s a lost cause. Yet the tide has begun to turn with a series of findings offering new insight — and revealing some tantalising new treatment possibilities.

Researchers at the University of Antioquia in Colombia are testing whether a drug called crenezumab can delay, or even stop, the condition in around 300 symptomfree Yarumal villagers who carry the mutation. The drug contains an antibody — a protein that locks onto a specific target — that destroys amyloid.

This is one of the key studies entering a new realm of research into preventing the condition, not just treating its symptoms.

‘I believe we are on the threshold of a breakthrough,’ says Lary Walker, an associate professor of neurology at emory University School of Medicine in the U.S.

And there is a whole portfolio of research revealing more about Alzheimer’s — from why catching a cold may hasten the disease to how injections of young blood can help. Here we round up some of the new findings that may finally solve the Alzheimer’s conundrum. A PROMISING SOLUTION . . . THe conventional view is that Alzheimer’s is characterised by proteins called amyloid beta and tau that misfold and build up into sticky plaques in the brain.

These proteins exist naturally — amyloid beta has a role in antimicrobial activity and the transport of cholesterol in the brain — but it is when their role is disrupted that they cause problems.

The plaques choke brain cells called neurons, preventing them passing on messages. They also trigger the destruction of healthy brain tissue. Scientists are discovering this can begin years before symptoms such as memory loss are noticeable. Understanding how this process starts may be key to preventing Alzheimer’s.

‘One of the challenges is that we still don’t know what normal physiological ageing looks like and how it compares to Alzheimer’s,’ says Delphine Boche, a professor of ne uroim mu no pathology at the University of Southampton. ‘We need to understand the normal changes much better in order to work out what is abnormal.’

The solution seems simple: clear these toxic proteins and fix the disease. Yet it is much more complex. No drug has managed to clear either protein effectively and stop the disease in humans.

In many cases, despite clearing plaques in animals, medicines fail in human trials due to side-effects such as brain swelling; or don’t lead to improved brain function.

But one drug — for now — appears to be bucking the trend.

In a small study by the developers, Biogen, involving 166 people, aducanumab, an antibody drug that like crenezumab binds to the misfolded amyloid and signals to immune cells to clear it from the brain, appeared to clear plaque and slow cognitive decline. It is the first to have a statistically significant effect on both cognition and volume of plaque. The results have been said to be ‘unusually robust’ by Alzheimer’s Research UK. But more trials are needed to determine its long-term efficacy, says professor Wilcock.

‘It’s too early to say whether it’s as promising as the manufacturer would have us believe.’ Larger trials have begun and if successful, it may be available within ten years. LOOKING IN THE WRONG PLACES SOMe scientists believe that plaques and tangles aren’t the whole story. For example, studies that have examined the Alzheim-