New Gains on the Frontier of the Battle Against Alzheimer’s Disease

March 31, 2012 § Leave a comment

A study published in the online Journal of Alzheimer’s Disease reports a critical discovery that will effect the development of new Alzheimer’s drugs as well as earlier detection for prevention. The FKBP52 protein may prevent the hyperphosphorylation of the Tau protein, keeping it from turning pathogenic.

The FKBP52 protein was discovered by Professor Etienne Baulieu twenty years ago. The hyperphosphorylation of the Tau protein is responsible for a number of cerebral neurodegenerative diseases, including Alzheimer’s Disease (AD). The current work is being carried out by Professor Baulieu and his research team at Inserm (National Institute for Medical Research in France).

It is believed that many neurodegenerative diseases are characterized by the accumulation of pathological hyperphosphorylated forms of Tau protein into structures called “Tau tangles.” Beyond this, there is limited knowledge about the Tau protein’s role in the development of AD. The means of Tau toxicity is uncertain so there are no drugs targeting the protein, nor any biomarkers that predict the risk of a future “Tauopathy”. Professor Baulieu and his team decided to concentrate on the Tau abnormalities. They were the first to discover, in 2012, an interaction between Tau and the FKBP52 protein.

The current research advances Baulieu’s previous research. It demonstrates a strong relationship between high levels of hyperphosphorylated Tau protein and reduced levels of FKBP52 in brain cells, from patients who have died as a result of Alzheimer’s Disease, compared with normal brain cells. This implies the anomalous production of pathogenic Tau is controlled by FKBP52 because when FKBP52 is reduced in the nerve cells of AD patients, pathogenic Tau accumulates and causes the degeneration of brain cells.

A basis for a predictive test for AD could be the early measurement of FKBP52 levels (before the onset of clinical symptoms). Also, new compounds that modulate FKBP52’s activity could develop into a new cohort of treatments for the disease.

Professor Baulieu said, “There is still a worrying lack of research into the causes of age-related brain disorders such as Alzheimer’s disease and dementia. I founded the Institut Baulieu with the aim of being able to treat and even prevent these diseases. Research on Tau has been very limited, and until recently, I was among the few scientists focusing on Tau pathology. The discovery of the FKBP52 protein is the only ‘anti-Tau’ perspective so far. Its reduced production in the brains of Alzheimer’s patients marks a turning point in understanding this complex disease. I believe it takes us one step closer to developing an effective treatment and possible predictive tests for the increasing number of people who may develop Alzheimer’s Disease in our ageing societies.”

Sources

“New Hope for Treating Alzheimer’s Disease: A Role for the FKBP52 Protein”. (March 20, 2012). Neuroscience News. March 24, 2012. http://neurosciencenews.com/fkbp52-protein-alzheimers-disease-anti-tau/.

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