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Prions may save you from Alzheimer’s disease

By Our Special Correspondent

“Until now, the normal function of prion proteins has remained unclear, but our findings clearly identify a role for normal prion proteins in regulating the production of beta-amyloid and in doing so preventing formation of Alzheimer's plaques. Whether this function is lost as a result of the normal ageing process, or if some people are more susceptible to it than others we don't know yet."


 

Proceedings of the National Academy of Sciences reported that there is a direct link between the presence of prions and prevention of Alzheimer’s disease. Prions are proteins that may cause mad cow disease if ‘corrupted’.

It is for the first time that there appears a link between the two. In case with the variant Creutzfeldt-Jakob disease (vCJD), type of ‘mad cow disease’ that affects human beings the Prions will appear corrupted.

Professor Nigel Hooper, who led the research group said, “Until now, the normal function of prion proteins has remained unclear, but our findings clearly identify a role for normal prion proteins in regulating the production of beta-amyloid and in doing so preventing formation of Alzheimer's plaques. Whether this function is lost as a result of the normal ageing process, or if some people are more susceptible to it than others we don't know yet."

This study paves way to new trials to develop a drug to cure the disease. There are reports that the protein may be used to prevent the disease – and not just for curing.

Professor Clive Ballard, director of research at the Alzheimer's Society said "These are early findings, which suggest prion proteins may have a regulatory effect on the development of beta amyloid. This provides the foundations for a novel approach to finding new therapeutic targets in Alzheimer's disease."

Now it is little known about the protein – Prion – especially its effects and significance. There could be a link between the aging process of the being and depletion of the protein content.

In the study the team found that the beta amyloid, the finite element of Alzheimer's "plaques" will not get built up if there is adequate presence of this protein. The fact that there are many similarities between Alzheimer's and diseases such as variant CJD, the research team is anticipating a strong link between them.

The team did the examination using a mice, genetically engineered one that was deficient in the prion level. The study has spurred up many researchers to take up the matter and to come up with a possible solution for the problem.

 

 


© Copyright 2007 The Analyst Magazine

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