Study: Missing Link Found Between Amyloid Beta and Tau

Northwestern University researchers have established a previously missing link between the two major brain abnormalities in Alzheimer's disease -- amyloid-beta and tau -- that may establish some common ground among researchers with disparate views on the disease.

For years, scientists have been debating whether the protein fragments amyloid-beta or the tangles of the protein tau are the major causes of Alzheimer's disease.

Recent findings have suggested that amyloid-beta, which surrounds neurons in the brain of Alzheimer's patients, prompts tau to assemble into tangles inside brain cells. But until now the actual mechanism by which this occurs was not well understood.

As reported in the online version of the Proceedings of the National Academy of Sciences, the researchers found that "suicide enzymes" known as caspases, a family of protein-cutting enzymes involved in programmed cell death, may be a direct link in the chain of molecular events leading to Alzheimer's disease.

Study co- authors Lester Binder and Vincent Cryns demonstrated that exposing neurons to amyloid-beta activates caspases, which split tau into smaller forms. The researchers then showed that this truncated form of tau was much more prone to forming abnormal filaments that resemble tangles, suggesting that amyloid exposure might promote tangle formation through the action of caspases on tau.

The researchers said their findings suggest the need to consider both of these interrelated events in future studies and therapies.

Other sources: Northwestern University