The research could lead to a viable treatment option for a range of neurodegenerative disorders, says an expert (Source: iStockphoto)Tuesday, 27 October 2009
Branwen Morgan

Blocking the action of a single enzyme prevents injured nerve cells dying and enables them to regrow, say scientists in the US. Their findings, to be published this week in the early edition of the Proceedings of the National Academy of Science, could have implications for sufferers of spinal injury and stroke, as well as neurodegenerative diseases such as Alzheimer's disease. The enzyme, called HDAC (histone deacetylase) belongs to a group known for their role in controlling gene expression - the creation of proteins based on DNA. Non-specific blocking of these enzymes causes most cells to die, but some nerve cells can survive. "We decided to try and find which of the HDACs could be selectively blocked to confer the neuroprotective effect without the unwanted toxicity", says Assistant Professor Brett Langley of the Weill Cornell Medical College in New York.

Process of elimination

The researchers used rat nerve cells grown in culture and tested several non-specific HDAC inhibitors to assess their neuroprotective ability during oxidative stress. Oxidative stress occurs in injured nerve tissue and is due to inflammation or loss of blood flow to the region. It can result in the loss of nerve cells for up to several weeks after the initial trauma. The inhibitors worked despite the presence of substances produced by the injured nerve tissue known to prevent the nerve cells repairing by themselves.

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The legacy of Marie Schlau: literature to help cure Friedreich's Ataxia

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Research projects currently being financed by BabelFAmily

Currently, BabelFAmily is financing two promising research projects aimed at finding a cure for Friedreich's Ataxia. Whenever you make a donation to us or purchase a copy of "The legacy of Marie Schlau", this is where all funds raised will be devoted to:

1) Gene Therapy for Friedreich's Ataxia research project:

The project is the result of an initiative of Spanish people affected by this rare disease who are grouped in GENEFA in collaboration with the Spanish Federation of Ataxias and the BabelFAmily. The Friedreich’s Ataxia Research Alliance (FARA), one of the main patients’ associations in the United States now joins the endeavour.

2) Frataxin delivery research project:
The associations of patients and families Babel Family and the Asociación Granadina de la Ataxia de Friedreich (ASOGAF) channel 80,000 euros of their donations (50% from each organisation) into a new 18-month project at the Institute for Research in Biomedicine (IRB Barcelona). The project specifically aims to complete a step necessary in order to move towards a future frataxin replacement therapy for the brain, where the reduction of this protein causes the most damage in patients with Friedreich’s Ataxia.

The study is headed by Ernest Giralt, head of the Peptides and Proteins Lab, who has many years of experience and is a recognised expert in peptide chemistry and new systems of through which to delivery drugs to the brain, such as peptide shuttles—molecules that have the capacity to carry the drug across the barrier that surrounds and protects the brain. Since the lab started its relation with these patients’ associations in 2013*, it has been developing another two projects into Friedrich’s Ataxia.



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