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Researchers discover hereditary enzyme deficiency
Date:6/13/2012

problems in finding the platform again. The defect is in the brain. In a study of tissue samples from the animals' cerebellum, the research team showed that through the accumulation of heparan sulfate, the Purkinje cells in the cerebellum die off and accompanied by inflammation are replaced by new cells. However, according to Dierks, these glia cells have only a supporting function and do not form any new connections to nerve cells.

A major success for the researchers is that their findings can be used to develop a treatment for this hereditary disorder and test this treatment on ARSG deficient mice. They are producing ARSG enzyme in a biotechnology process with the help of genetically modified cell cultures. In sick mice that are regularly injected with a solution containing the enzyme, further damage to their organs should be stopped, Dierks believes. Similar treatments are successfully applied to patients with other mucopolysaccharidosis disorders. 'The biochemical processes underlying such lysosomal storage disorders are principally the same in all mammals. However, effects are more severe in human beings because of their greater life span', says Dierks. An early diagnosis of these disorders can be difficult because the onset is frequently insidious. Sometimes, the disorder can only be recognized through its symptoms in adolescence. And then the diagnosis is difficult for a physician, Thomas Dierks says, 'because systematic screenings are performed only in childhood, and one does not initially consider a genetic cause. However, treatment has to start as early as possible'. 'Dierks's disorder' can be diagnosed unequivocally with a mass spectrometer the researchers have developed their own procedure for this.


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Contact: Prof. Dr. Thomas Dierks
thomas.dierks@uni-bielefeld.de
49-521-106-2092
University of Bielefeld
Source:Eurekalert  

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