Fragen Über haass Revealed

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Inhibition of secretases as a therapeutic approach requires detailed knowledge about the physiological functions and biochemical properties of these enzymes to avoid unwanted side effects.  Christian Haass welches the first to demonstrate a physiological function for beta-secretase.  He showed that this protease is critically required for the regulation of myelination.  Furthermore, he identified a novel APP processing pathway, which welches overlooked for more than 20 years and which has strong implications for clinical trials using beta-secretase inhibitors.  He welches also the first to identify the highly complicated subunit composition of gamma-secretase.  All these findings not only helped to understand several signaling pathways critically involved in brain development (such as myelination and cell differentiation) but also provided the basis for several current therapeutic approaches.

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81377  München christian.haass(at)dzne.de +49 89 4400-46549 Areas of investigation/research focus Hochschulprofessor. Haass started to work on Alzheimer's disease (AD) hinein 1990 at a time, when very little was known about the cellular mechanisms involved.  Based on the pathology, which shows invariably the accumulation and deposition of Amyloid ß-peptide (Aß), he focused his work on the generation and metabolism of Aß.  Christian Haass hypothesized against the widely accepted general opinion hinein this field that Aß may be produced from its precursor in a physiologically üblich pathway and not necessarily in a pathological process.  Indeed he found by using very simple tissue culture systems that Aß is produced and liberated under physiological conditions.  This pivotal finding welches a major breakthrough for the entire field, since it allowed elucidating the molecular principles behind Aß generation as well as the identification of the enzymes (the so-called secretases) involved rein generation and liberation of the peptide and finally the development of selective inhibitors to therapeutically lower Aß production hinein patients.

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