WASHINGTON, Feb. 7 (Xinhua) -- A new study tried to redefine the causes of Alzheimer's disease (AD), arguing that it is likely triggered by the failure of a system that clears wastes from the brain and begins decades before memories fade.

The findings, published Wednesday in the journal PLOS ONE, demonstrate that the current biological understanding of the chronic neurodegenerative disease is incomplete. In the past 25 years, people focus on the build-up in brain tissues of a protein called amyloid beta.

Researchers at the NYU School of Medicine suggested that standard diagnostic tools fail to catch future AD in many patients younger than age 70.

In the commonly held definition of Alzheimer's disease, one type of amyloid beta starts to form clumps between nerve cells and injure those cells, and worsening injury is then marked by the release and toxic buildup of a second protein called tau.

Together, changes in amyloid beta and tau levels represent the standard international measure of a patient's risk for future cognitive decline.

The new study, however, found that the increase of amyloid beta cannot be the sole trigger of subsequent nerve damage because many relatively younger people who develop disease later do not show signs of the buildup.

"By recognizing an earlier disease phase, we may be able to start treating earlier and in tailored ways based on a better understanding of disease biology," said lead study author Mony de Leon, director of the Center for Brain Health, at New York University.

In 1999, de Leon and colleagues started collecting protein level data in cerebrospinal fluid (CSF) that fills the spaces around brain tissue from healthy normal subjects every two years.

The study found that the best predictor of future AD risk was not decreased CSF amyloid beta levels, which is taken as evidence of a buildup in brain cells, with elevated tau. Elevated CSF amyloid beta levels were also found to confer future AD risk.

By including in AD risk prediction models patients with either rising or falling CSF amyloid beta, along with steadily rising tau, the team increased the accuracy of future risk prediction by nearly 20 percent higher than current models, which only consider falling levels.

The improved accuracy was even more pronounced in those aged younger than 70 years, de Leon says.

Although the actual mechanism behind Alzheimer's disease and the trajectory of amyloid beta and tau levels remains obscure, the results provide evidence in support of the "clearance theory."

The theory holds that the pumping of the heart, along with constriction of blood vessels, pushes CSF through the spaces between brain cells, clearing potentially toxic proteins into the bloodstream. But mid-life cardiovascular changes may lessen the CSF flow needed to clear tau.