The research held by the Jerusalem Jewish University led to new and perspective way to Alzheimer disease treatment.

Throughout the research the scientists of Biologic Science Institute at the Jewish University revealed the secret of why people having mutated BChE-K genom are disposed to faster Alzheimer disease development comparing to those having normal genom. This mutation appears in 20% Americans and Israeli.

In theory those having this mutated genom should be less disposed to the disease as the mutated protein destroys neurotransmitter acetylcholine slower then in those having normal genom. As a result the genom carriers have increased neurotransmitter level thus they should be more protected against the Alzheimer disease that is characterized by the decrease of the acetylcholine level.

In fact these carriers are disposed to later than in other people development of the disease. However when this occurs the disease develops faster and doesn’t reacts the medications intake. Thus the main point is that the mutated genom carriers are disposed to greater risk of the disease development than other people.

The reason of this uncommon situation was in secret for many years but the research of the Jewish University scientists revealed it and explained this high risk and proposed possible therapeutic solution. The researchers of the Wolfson Structure Biology Center at the Jewish University revealed that the BChE-K genom mutation damages the end (tail) of the enzyme protein appeared as the mutation result. This tail is the BChE part required for Alzheimer disease plaques protection.

In order to compare normal protein with K-mutant the researchers used synthetic K-protein and normal BChE tails obtained by the American company «Pharmathene» from the transgenic goats’ milk. The protein obtained from goats was prepared by the «Pharmathene» company for the use in the US military Forces as the protection against the nerve-paralytic gas. This protein turned to be more stable and effective than the mutant protein. This means that the disposition of the BChE-K carriers to the Alzheimer disease may be considerably improved by the treatment with the normal protein obtained from the transgenic goats’ milk.