A discovery that the presence of prions interrupts the buildup of beta amyloid may point to new therapies to treat Alzheimer's. The research work was triggered by similarities between human mad cow disease and Alzheimer's. In mad cow disease, corrupted prion proteins cause brain damage. When the level of normal prions is high, the researchers noted, the presence of beta amyloids was low. When the level of prions was low, though, beta amyloids were more prevalent. To test the work, researchers used a mouse model designed to eliminate normal prions. Those mice developed new formations of beta amyloid.

Next researchers will examine whether the aging process interferes with prion proteins' ability to protect people from the build up of beta amyloids. A new therapy that mimics the effects of prions could theoretically be used to stop the development of the disease.

- see the release [1]
- read the BBC's report [2]

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