In the study, three different mice models of Alzheimer's disease were treated with an already FDA approved drug. Their beta amyloid plaque melted away and the mice had return of cognitive function. And since it was an approved drug, we may know very quickly if this works in humans.

Your brain cells put out waste products in the form of beta amyloid protein. Normally, Apo E genes act like garbage trucks collecting and removing this toxic waste from the diseased brain.

If one of the two Apo E genes you inherit is mutant or dysfunctional, your risk of Alzheimer's disease goes up about 30%. If both are, it goes up more than 60%. Lack of function of this gene leads to Alzheimer's disease. That is how these mice were created - they were literally designed to mimic this Apo E genetic defect.

When the Case investigators gave this drug to the mice, it turned on the Apo E gene, making it more active - 25% of beta amyloid disappeared in the first day and 75% of it in three days. If you extrapolate that to human studies, that would be the same thing as 75% of that plaque disappearing in 100 human days. But more importantly, brain cognition (in mice, the ability to have nesting behavior and the ability to sense smells) returned.

So, what is the holdup in trying this in humans? Very little. The drug is Bexarotene, which is made by a small company for a specific cancer diagnosis. It causes thyroid and blood cell problems in some, birth defects, kidney failure and some other not-so-pleasant things.

So, what remains for human testing? First, repeating the test results in mice - that is now under way at Cleveland Clinic and University of Chicago, among others, so we should know that soon.

Go to full story: http://www.clevelandjewishnews.com