Build-up of a harmful protein in the brain can predict atrophy in Alzheimer's disease patients at least one year in advance.
Previous studies have shown that two tell-tale plaques, amyloid beta and tau, form clumps that smother and destroy neurons.
But researchers found that only accumulation of the tau protein was indicative of where damage would occur as Alzheimer's progressed.
The team, from the University of San Francisco Memory and Aging Center, says the findings shed fresh light on the age-related brain disease and that either drugs could prevent this neurodegeneration or that scans predicting future atrophy could lead to personalized dementia care.
A new study from the University of San Francisco has found that levels of tau protein in the brain were more predictive of future degeneration compared to amyloid proteins in Alzheimer's patients (file image)
'No one doubts that amyloid plays a role in Alzheimer's disease,' said lead author Dr Renaud La Joie, a postdoctoral researcher at the University of San Francisco.
'But more and more tau findings are beginning to shift how people think about what is actually driving the disease.'
It is estimated that there are about 44 million people worldwide - 5.7 million of whom are Americans of all ages - living with Alzheimer's disease.
The progressive brain disorder slowly destroys memory, thinking skills and the ability to perform simple tasks.
There is no known cure for Alzheimer's, but experts suggest physical exercise, social interaction and adding brain boosting omega-3 fats to your diet can slow down the onset of symptoms.
Such symptoms can include disorientation, difficulty remembering newly learned information and suspicion about family and friends.
Scientists have debated for years the importance of amyloid beta proteins and tau proteins, which were discovered in the early 20th century.
Numerous drugs have been manufactured attempting to target amyloid, with mixed or few results.
This has led to researchers looking at tau - which was once seen as just an indication of where brain cells had died - to see if this protein is actually driving the disease.
For the study, published in the journal Science Translational Medicine, the team recruited 32 people with early stage Alzheimer's disease.
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