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Recently discovered protein shows promise in treating Alzheimer’s diesease

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New research in humans shows that the FKBP52 protein may prevent the Tau protein from turning pathogenic, or from causing disease.  

The FKBP52 protein was discovered by Baulieu 20 years ago in its ability to block Tau protein accumulation, which is commonly seen in Alzheimer’s disease (AD)patients. Microtubules are the railways in the brain upon which cellular cargo is transported. In patients with AD, tau tangles formed by misfolded tau proteins may compromise the stability of the microtubules within the nerve cells leaving them damaged. Currently, the mechanism of Tau toxicity is unclear and there are no drug treatments targeting Tau.

Professor Etienne Baulieu and colleagues at Inserm (National Institute for medical research in France) have recently published results that for the first time demonstrate that the FKBP52 protein may prevent hyperphosphorylation, or over accumulation of Tau protein, a characteristic of Alzheimer’s disease.

Specifically, the results of this study demonstrate a direct correlation between high levels of hyperphosphorylated Tau protein and reduced levels of FKBP52, in brain cells from patients that had died following AD, compared to normal brain cells. This indicates that when FKBP52 is reduced in nerve cells of AD patients, disease causing Tau is free to accumulate and contribute to the degeneration of brain cells.

References
IOS Press BV (2012, March 20). New hope for treating Alzheimer’s Disease: A Role for the FKBP52 protein. ScienceDaily. Retrieved April 5, 2012, from http://www.sciencedaily.com/releases/2012/03/120320195338.htm     
 
Julien Giustiniani, Marlène Sineus, Elodie Sardin, Omar Dounane, Maï Panchal, Véronique Sazdovitch, Charles Duyckaerts, Béatrice Chambraud, Etienne-Emile Baulieu. Decrease of the Immunophilin FKBP52 Accumulation in Human Brains of Alzheimer’s Disease and FTDP-17. Journal of Alzheimer’s Disease, Volume 29, issue 2 (March 2012) [link]

 


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