A predicted exodus of European doctors, nurses and care workers following Brexit will be disastrous for Alzheimer’s patients and their families, according to a pioneering dementia scientist who was on Tuesday named as a joint recipient of the world’s most prestigious prize in neuroscience.

Speaking at a press conference in London ahead of the announcement of the winners of the 2018 Brain prize, Prof John Hardy, of University College London, described the UK leaving the EU as an “unmitigated disaster for science and an unmitigated disaster for the health service”, adding that he planned to donate some of his prize money to the anti-Brexit campaign group Best for Britain.

Hardy shares the €1m prize from the Lundbeck Foundation in Denmark with Prof Bart De Strooper, director of the UK Dementia Research Institute at University College London, Prof Michel Goedert of the Medical Research Council Laboratory of Molecular Biology in Cambridge and Prof Christian Haass of the Ludwig-Maximilians-University of Munich. Together the scientists helped map out the genetics and biological processes that underpin the devastating effects of Alzheimer’s.

Hardy said NHS services have already been left “close to collapse” because, as the number of patients with dementia in the UK has risen to nearly 1m, funding has not kept pace. If doctors and care staff leave the country in significant numbers the system will be placed under even more severe pressure, Hardy said.

“When you go around the hospitals, so many of the geriatricians and neurologists are Europeans, and the nurses and carers,” he said. “As a society we’re not doing very well, and the indications are we’re going to do even worse.”

Hardy described the field of dementia research that he encountered in the early 1980s as “a real backwater” and said extraordinary progress on understanding the pathology of the disease had been made since then. “The first conference only attracted 40 people, but now thousands attend,” he said.

In the late 1980s, Hardy’s team at UCL began studying a family from Nottingham who had been blighted by early-onset Alzheimer’s for several generations. Blood tests uncovered a genetic mutation in a stretch of DNA linked to the production of amyloid protein.

“We put that pathology into order,” he said. “Instead of basically seeing a car crash of pathology we could say that happened first.”

De Strooper further advanced the so-called amyloid hypothesis by identifying the role of a protein, presenilin, that “cuts” other brain proteins into smaller segments. De Strooper showed that a faulty version of the presenilin gene results in the production of an abnormal version of amyloid, leading to the formation of tangles and sticky plaques in the brain.

Together, the findings suggested that if a drug could be found to block the production of amyloid or stop its accumulation, the disease might be slowed or prevented.



However, 30 years on, no drug has been shown to slow the progression of the disease – current treatments only alleviate symptoms. Successive failures of drug trials have led to many pharmaceutical companies – most recently Pfizer – pulling the plug on their neuroscience programmes.



Hardy describes this as a “great disappointment”. “Things are more hopeful now from a scientific point of view and an understanding point of view than they were five years ago,” he said. “I think pharma is making a mistake pulling out.”

The successive trial failures have led some to question whether the amyloid hypothesis is misguided but Hardy believes it should remain a focus, arguing that many of the failures could be down to trials involving patients who are already in the late stages of disease. More recent research suggests that amyloid can start accumulating in the brain 15-20 years before symptoms occur. “It’s like popping a statin to treat a heart attack – the right drug but the wrong time,” he said.

Goedert discovered that along with amyloid, another protein, tau, is implicated in Alzheimer’s and other neurodegenerative diseases.

Haass’s lab has produced a series of breakthroughs that allowed scientists to link together the cascade of biological steps, starting with amyloid production, the development of plaques and the eventual death of neurons that result in memory loss.



Haass said he hoped the prize would put a spotlight on the potential for science to lead to social good. “We are facing a time when more and more people don’t believe in science any more,” he said. “Science is not always right, but it is the only way to go to find the truth and for humans to progress.”

The scientists will be presented with the prize on 9 May in Copenhagen by Crown Prince Frederik of Denmark.

