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Alzheimer’s disease is back in the headlines with the announcement that the annual €1 million has gone to four neuroscientists researching the genetic and molecular basis of the illness.

This is recognition of great basic science. at University College London (UCL) was the first to propose that Alzheimer’s disease was initiated by the build-up of beta amyloid, a protein that can coagulate into plaques that kill brain cells. at the Medical Research Council Laboratory of Molecular Biology in Cambridge, UK, was instrumental in the discovery of the importance of tau protein, which also forms damaging plaques.

Their work, along with that of at the Ludwig Maximilian University of Munich, Germany, and at UCL, has added to our knowledge about the underlying mechanisms of dementia.

The prize, awarded by the Lundbeck Foundation in Copenhagen, Denmark, will undoubtedly raise hopes that a cure for Alzheimer’s disease is within our grasp. However, translating such research, much of it in animals, into drugs that work in humans remains as frustratingly out of reach as ever.

There are 850,000 people with dementia in the UK alone, set to rise to over a million by 2025 and over 2 million by 2051. Worldwide, someone develops dementia every 3 seconds. For these people and their families desperate for a breakthrough, it has been a long roller coaster of raised hopes and crushing disappointments.

Again and again there has been feverish excitement in the media over a potential cure. A drug that looks promising in mice leads to overblown headlines, yet when it reaches phase III studies in humans the results are disappointing.

Multiple failures

The disheartening reality is that there has been no new drug for dementia in the past 15 years. Instead we have seen a long line of failures. Of 214 compounds tested between 2000 and 2014, only one was ever licensed – a failure rate of 99.6 per cent.

For example, there were high hopes that solanezumab – a monoclonal antibody targeting amyloid plaques – would be the first to slow down the progression of Alzheimer’s disease. But in November 2016 a clinical trial found it produced no meaningful benefit for people with the condition.

Some have suggested that researchers are following the wrong path by focusing on amyloid. We know that amyloid starts being deposited in neurons up to 20 years before the onset of Alzheimer’s, so by the time symptoms appear it may be too late.

Recently there has been more attention paid to the role of tau proteins, which form tangles in the brains of people with Alzheimer’s disease. However, in summer 2016 hopes were dashed when the experimental tau-targeting drug LMTX failed to help Alzheimer’s patients.

In January this year there was yet another disappointment when another experimental drug, idalopirdine, in a series of three trials. The drug largely acted to increase levels of serotonin along with four other neurotransmitters that are affected by Alzheimer’s, and had looked promising in earlier safety trials. The failure probably closes the door on another approach to Alzheimer’s treatment.

With such a high failure rate, it is no surprise that the drug giant Pfizer announced in January that it is .

The G7 countries set a target of finding a disease-modifying treatment for Alzheimer’s by 2025, but this is sadly looking unlikely to happen. Honouring the hard work on this illness with the Brain prize is great – just don’t expect rapid breakthroughs.