Drug Trial Fails To Slow Memory And Thinking Decline In Rare Genetic Form Of Alzheimer’s

Scientists have announced results from DIAN-TU, an international clinical trial testing the potential Alzheimer’s drugs, solanezumab and gantenerumab, in people with a rare, inherited form of Alzheimer’s disease. The drugs failed to have a meaningful benefit on memory and thinking in people with familial Alzheimer’s disease (FAD).

Dr Carol Routledge, Director of Research at Alzheimer’s Research UK:

“Today is hugely disappointing, particularly for people with familial Alzheimer’s but also for the millions of people who may develop the more common, non-genetic form of the disease. While there has been no meaningful benefit to people’s memory and thinking when taking either drug in this trial, we must not lose sight of the urgent need for effective dementia treatments.

“Investigating drugs like this in people with rare-inherited forms of Alzheimer’s disease is a crucial step in bringing about new drugs and this innovative trial is set to continue. At present we only have headline results and need to see the data in full before we can understand what this means for future trials.

“While these drugs did not have the effect that we hoped for, it is vital that we continue to explore every avenue in the search for new ways to help people with Alzheimer’s. We know that the diseases that cause dementia can occur up to two decades before symptoms show and working with people who have rare, inherited forms of Alzheimer’s disease remains an important approach in bringing about new drugs.

“I would like to thank all the volunteers who take part in dementia research, whose sustained and dedicated efforts are pivotal to making breakthroughs possible. We are particularly grateful to the unique group of brave participants who took part in this trial, who have made an important contribution to research that will improve our understanding of the disease and ultimately change lives.

What is the DIAN-TU trial?

The DIAN-TU – the Dominantly Inherited Alzheimer Network Trials Unit – is an international drug trial to see whether the rare genetic form of Alzheimer’s – familial Alzheimer’s disease (FAD) – can be slowed down by potential new medicines.

Scientists tested two potential drugs – solanezumab and gantenerumab – both targeting amyloid, the hallmark Alzheimer’s protein.

Participants in the trial were from around the world, including a centre at University College London in the UK. Volunteers either knew they have an Alzheimer’s disease-causing mutation or were unaware of their genetic status but had a FAD mutation in their family.

Why is this study important?

DIAN-TU is the first study of its kind, testing the use of antibody drugs to prevent or slow down the onset of Alzheimer’s in those who have a genetic risk of developing this disease early in life. There are currently no treatments available on the market to do so.

A build-up of amyloid around brain nerve cells is thought to start a cascade of processes leading to the death of nerve cells and eventually a loss of memory.

The drugs

Solanezumab and gantenerumab target this protein. Both drugs have had a chequered history and both work in slightly different ways.

Solanezumab is designed to clear clumps of amyloid from the brain, and gantenerumab is designed to stop the large build-up of amyloid forming.

The way both drugs are given is also different. Solanezumab is given by infusion and gantenerumab was given as a monthly injection. The drugs were given in increasingly higher doses over a period of four years.

What did the study show?

The study failed to show benefit to study volunteer’s memory and thinking. We don’t yet know whether they had any other benefits.

How common is a genetic form of Alzheimer’s disease?

About one percent of people with Alzheimer’s disease will have the genetic form, known as familial Alzheimer’s disease (FAD).

It is genetically inherited or passed down through families. Individuals who have a parent with a genetic mutation have a 50 percent chance of carrying the gene and many experiences an onset of symptoms in their 30s and 40s.

 

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