Researchers have been able to see the deadly chain reaction at the start of the incurable disease which causes the death of nerve cells.
Powerful new imaging techniques suggest tau spreads across the brain, infecting and destroying nerve cells as it goes, causing symptoms to get progressively worse.
Confirmation is crucial because it indicates the progression of Alzheimer’s could be slowed down, or even halted, by developing drugs to stop tau in its tracks.
Study author Dr Thomas Cope, of the Department of Clinical Neurosciences at the University of Cambridge, said: “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. It’s the same as we might see in a flu epidemic, for example – the people with the largest networks are most likely to catch flu and then to pass it on to others. And this is exactly what we saw.”
Until recently it was only possible to look at the build-up of proteins by examining the brains of patients who had died. But advances in positron emission tomography (PET) scanning enabled scientists to trace their build-up in patients who are still alive.
In the study, the results of which are published in the journal Brain, 17 Alzheimer’s patients were injected with a radioactive ligand, a tracer molecule that binds to tau and can be detected using a scanner.
Professor James Rowe, senior researcher, said: “In Alzheimer’s, the most common brain region for tau to first appear is the entorhinal cortex area, which is next to the hippocampus, the ‘memory region’.
“This is why the earliest symptoms in Alzheimer’s tend to be memory problems.
“But our study suggests tau then spreads across the brain, infecting and destroying nerve cells as it goes, causing the patient’s symptoms to get progressively worse.”
Around 500,000 are now living with Alzheimer’s, the most common form of dementia, in the UK.
Symptoms include memory problems, changes in behaviour and progressive loss of independence.
They are caused by the build-up of two abnormal proteins: amyloid beta and tau.
It is thought amyloid beta occurs first, encouraging the appearance and spread of tau which then destroys nerve cells, eating away at memory and mental function.
How tau appears throughout the brain has been the subject of fevered speculation.
Some believe it is made locally in nerve cells while others think some brain regions are more vulnerable than others.
Scientists now think it is possible to develop drugs to stop it from moving along neurons, a process known as the transneuronal spread hypothesis.
Dr Doug Brown, director of research and development at Alzheimer’s Society, said: “Better images of tau would mean earlier and more accurate diagnosis of Alzheimer’s and other forms of dementia.
“Being able to see the tau protein in the living brain would also help in the search for new treatments, as researchers could use this to see whether a treatment is successfully targeting tau.”