Promising new treatment for Alzheimer's suggested based on Hebrew Universit...( Research carried out at the Hebrew U...)

Research carried out at the Hebrew University of Jerusalem has resulted in a promising approach to help treat Alzheimer's disease in a significant proportion of the population that suffers from a particularly rapid development of this disease.

In the research at the Silberman Institute of Life Sciences of the Hebrew University, scientists solved a mystery as to why people who carried a mutated gene known as BChE-K were prone to more rapid development of Alzheimer's than those who had a normal version of the gene. This mutation appears in about 20 percent of the American and Israeli populations.

In theory, the carriers of the mutated gene should actually be more protected from the devastating effects of the disease, since the mutated protein (the enzyme that is the product of the gene) breaks down the neurotransmitter acetylcholine at a slower rate than in those who have the normal gene. The result is that the carriers maintain higher levels of this neurotransmitter, so they should in principle be protected from Alzheimer's disease, in which acetylcholine levels decrease.

Indeed, these carriers tend to develop the disease later than others, but when that happens, it progresses more rapidly and does not respond to medication. Therefore, the bottom line is that carriers of the mutated gene have a greater risk than others for disease progression. The reason for this anomalous situation has been a puzzle for a long time, but the studies by the Hebrew University scientists solved it by finding the explanation for this increased risk, thereby offering as well a possible new therapeutic solution.

At the Wolfson Center for Structural Biology at the Hebrew University, the researchers found that the mutation in the BChE-K gene damages the very end, or tail, of the resultant mutant enzyme protein. This tail is the part of BChE which is important for protection from the Alzheimer's disease plaques. It does this by interacting with the
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