Recent advances in brain imaging have enabled scientists to show for the first time that a key protein which causes nerve cell death spreads throughout the brain in Alzheimer's disease – and hence that blocking its spread may prevent the disease from taking hold.

An estimated 44 million people worldwide are living with Alzheimer's disease. Its symptoms are caused by the build-up in the brain of two abnormal proteins: amyloid beta and tau. It is thought that amyloid beta occurs first, encouraging the appearance and spread of tau. It is this latter protein that destroys the nerve cells, eating away at memories and cognitive functions.

Until a few years ago, it was only possible to look at the build-up of these proteins by examining the brains of Alzheimer's patients who had died. However, recent developments in positron emission tomography (PET) scanning have enabled scientists to begin imaging their build-up in patients who are alive: a patient is injected with a radioactive ligand, a tracer molecule that binds to the target (tau) and can be detected using a PET scanner.

In a new study, a team led by University of Cambridge scientists describe using a combination of imaging techniques to examine how patterns of tau relate to the wiring of the brain in 17 patients with Alzheimer's disease, compared to controls.

How tau appears throughout the brain is the subject of speculation. The “transneuronal spread” hypothesis says harmful tau starts in one place and then spreads to other regions, setting off a chain reaction. The “metabolic vulnerability” hypothesis says that tau is made locally in nerve cells, but that some regions have higher metabolic demands and hence are more vulnerable to the protein. The third hypothesis, “trophic support,” suggests that some brain regions are more vulnerable than others because of a lack of nutrition to the region or because of gene expression patterns.

Thanks to the developments in PET scanning, it’s now possible to compare these hypotheses.

"Five years ago, this type of study would not have been possible, but thanks to recent advances in imaging, we can test which of these hypotheses best agrees with what we observe," says Thomas Cope from the Department of Clinical Neurosciences at the University of Cambridge, the study's first author.

Cope and colleagues looked at the functional connections within the brains of the Alzheimer's patients and compared their findings against levels of tau. What they found supported the idea of transneuronal spread – that tau starts in one place and spreads. "If the idea of transneuronal spread is correct, then the areas of the brain that are most highly connected should have the largest build-up of tau and will pass it on to their connections."

Confirmation of the transneuronal spread hypothesis is important because it suggests that it might be possible to slow down or halt the progression of Alzheimer's disease by developing drugs to stop tau from moving along neurons.