ALZHEIMER'S: A discovery "surprise" that can block the disease

A discovery "surprise" has enabled the researchers from University College Dublin to block the Alzheimer's disease. By chance, or almost, these scientists seeking treatment for Creutzfeldt-Jakob disease (CJD) have blocked the development Alzheimer's disease. Targeting prion proteins responsible for the development of CJD, thus preventing the binding bêta-amyloïde/prion, researchers can block the accumulation of beta-amyloid protein in the brain responsible for development of Alzheimer's. The scientists were able to isolate two antibodies targeting CJD that may well "work" also for Alzheimer's. Results published in the June 7 edition of Nature Communications.

The study in question is currently a lab experiment on animals to study the association between two types of proteins. One of the proteins studied, the protein beta-amyloid, accumulates in Alzheimer's disease. An abnormal form of another protein, the prion protein is responsible for CJD. Scientists have discovered that blocking the connection between these two proteins prevents the protein beta-amyloid block nerve signals. On samples of mouse brain and in the brains of live rats. Alzheimer's disease is a complex disease, caused by the death of nerve cells in certain brain regions. What triggers the death of nerve cells is not yet fully understood and block the effects of amyloid protein might not be sufficient to prevent apoptosis of neurons. All that remains yet to be validated.

Nevertheless, the interesting point of this study is to suggest that it might be very interesting to test antibodies that target prion proteins in Alzheimer's disease. These antibodies have already been developed to treat MCJpourraient be tested relatively quickly, in humans, in the case of Alzheimer's disease.

This animal research has examined the interaction between two proteins involved in brain damage reached Creutzfeldt-Jakob disease (CJD) and Alzheimer's disease. These two proteins studied, the protein beta-amyloid and prion protein are present in normal brain tissue, but strongly involved in these 2 diseases. It is known that the accumulation of beta-amyloid contributes to the death of neurons in the brain, which causes symptoms of the disease. Previous research has
suggested that the protein beta-amyloid may need to bind to prion protein to cause this adverse effect on the function of neurons. The researchers therefore examined the association using blocking antibodies, special proteins that the immune system uses to defend the body. The researchers found that two anti-prion, called ICSM-18 and ICSM-35, already tested in CJD could block the binding of beta-amyloid with the prion protein. These antibodies have also been able to stop the effect of accumulation of the protein beta-amyloid. ICSM-18, in particular, has demonstrated, long term and live rats, its potential for blocking the accumulation of the protein.

This type of study therefore suggests a new therapeutic target for possible new treatments for Alzheimer's disease. These treatments can be tested in laboratory, animal, trying to identify which are most promising for testing in humans.

Cinnamon against Alzheimer's?

Initially, the team of Prof.. Ovadia had noticed that this compound from cinnamon slowed significantly the progression of diseases such as flu or herpes. Then they got the idea to experiment with cells with Alzheimer's. This molecule called CEppt "has been applied to laboratory mice inoculated cells of aggressive disease, similar to those found in the brains of people with Alzheimer's disease. They were watered regularly then a mixture containing this molecule "CEppt" extracted from cinnamon bark. The researchers then observed by electron microscopy that the molecule had slowed the production of amyloid protein, which is one of the major elements of the evolution of Alzheimer's disease to the point that genetically engineered animals have found a behavior similar to their "fellow" healthy.
Experience has shown by example that the "CEppt" had not only managed to slow down to prevent the proliferation of diseased cells, but also to disintegrate the new cells amyloid.
Team's conclusion: this natural product may be liable not only to repel or prevent the onset of the disease, but also the set back when it is already apparent. But Prof. Ovadia wants to remain the "grounded" and recalls that "it is still only preliminary experiments conducted on laboratory animals."
He advises to consume products containing cinnamon tea as such, "but certainly not rushing into stores and spices to swallow spoonfuls of cinnamon, because the excess of this product is harmful to liver ."

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