Scientists researching the causes of Alzheimer's disease say it may not be plaque, long considered the prime suspect, but rather protein than steals a person's memory and interferes with behavior and thinking by killing brain cells.

Both plaque consisting of amyloid-beta protein fragments and tangles of a protein known as tau are seen in the disease, but Georgetown University Medical Center researchers say they've found evidence it's the tau rather than the plaque that accelerates neuron death.

This could be the reason why some people with significant plaque build-up within their brains don't show any signs of dementia, and the findings could also lead to new drugs that could treat Alzheimer's, the researchers report in the journal Molecular Neurodegeneration.

"For a very long time, we believed, for almost 100 years, that [amyloid-beta] plaques are the main culprit in Alzheimer's disease," study senior investigator Charbel E-H Moussa says. "This study shows it's another protein -- a very, very important one, called tau, that is basically the main guilty one."

Inside a brain cell, tau provides a structure, something akin to a train track, which allows the cell to dispose of accumulations of unwanted toxic proteins.

If tau stops functioning -- possibly from aging or from errant genes -- the cell is unable to rid itself of the toxins.

Contrary to previously belief, it is the protein the cells can't dispose of and that remains inside neurons that causes them to die, not the plaques that build outside of the cells, the researchers say.

As part of their investigation, the researchers looked at the anti-cancer drug nilotinib, approved for used in adult leukemia patients, as a possible treatment to clear out such intercellular debris and control levels on nonfunctioning "bad" tau.

Nilotinib works by entering a cell to help clear it of debris, but can also reduce plaques building up outside the cell, says Moussa, who hopes to start clinical trials within weeks.

The discovery of the role of tau in Alzheimer's could lead to screening that could uncover signs of the disease at an earlier state and and help predict if a patient is likely to develop dementia, he says.

"Recent evidence suggests it appears that tau modification happens much earlier than amyloid plaques ... and because almost every patient who has tau modification has dementia, it's going to be a much more reliable and precise predictor of Alzheimer's and other dementias than [amyloid-beta]," Moussa says.

Such screening in combination with drugs that can reduce non-functioning tau in brain cells could slow down further tau breakdown and plaque buildup, helping patients avoid Alzheimer's or dementia, he adds.

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