The causes of Alzheimer’s Disease are not fully understood but scientists agree that two proteins contribute to its development. One is amyloid, which is a fragment of a protein and the other is tau, which is a full protein. The accumulation of each is associated with the onset of cognitive decline.

In recent years the first treatments have been developed which have some (limited) ability to slow down disease progression. However, these only target amyloid build-up. One reason why we remain unable to make a bigger impact on this terrible disease might be that we have no tools to tackle tau.

This could be about to change.

Scientists have demonstrated, in autopsy samples from deceased patients, that a short peptide can wrap itself around tau fibrils and break them up. Although it is quite hard to develop treatments which can cross the blood brain barrier and work effectively in the brain, this one shows promise by deploying magnetic nanoparticles which help it infiltrate the brain. The drug doesn’t have a name yet, but the peptide which has the demonstrated effect is catchily referred to as D-TLKIVWC12¹.

Tau begins to accumulate many years before Alzheimer’s becomes symptomatic, and in theory intervention in this window (i.e. of up to 10 years) could help slow progression, though whether this would be the case in live humans, and the magnitude of any impact remain uncertain.

It remains the case that most instances of Alzheimer’s are not diagnosed until a much later stage. This is another potential reason why drugs tackling amyloid might not work well – maybe they’re being delivered too late. It means that any drug emerging from these new findings would likely be just one part of wider efforts to identify and slow this disease, and is only likely to have an impact if we also develop – and widely use! – reliable tests on people who are asymptomatic.

¹ How short peptides disassemble tau fibrils in Alzheimer’s disease | Nature