81377 München christian.haass(at)dzne.de +49 89 4400-46549 Areas of investigation/research focus Prof. Haass started to work on Alzheimer's disease (AD) rein 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 in this field that Aß may be produced from its precursor rein a physiologically normal 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 was 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 hinein generation and liberation of the peptide and finally the development of selective inhibitors to therapeutically lower Aß production rein patients.
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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 was 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 was 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 hinein brain development (such as myelination and cell differentiation) but also provided the basis for several current therapeutic approaches.
You are allowed to have 10 minus points. You have failed the test if you get 11 or more minus points. If you incorrectly answer two questions each with five minus points, you have also failed the test in spite of not exceeding the maximum number of minus points; rein Class B, questions with 5 points have a greater relevance rein the theoretical test.
Very recently he also investigated the role of microglia and inflammation in neurodegenerative disorders. This work led to the spectacular finding that microglial phagocytosis may Beryllium impaired late during neurodegeneration and opened up a completely unexpected road towards new therapeutic developments for patients already developing disease symptoms. This work resulted hinein the identification of TREM2 as a CSF marker for microglial activity. In a unique cohort of subjects with autosomal dominant AD, CSF sTREM2 welches abnormally increased 5 years before the expected onset of symptoms. This will not only greatly facilitate research on inflammatory disease overarching mechanisms, but may also provide a very valuable therapeutic marker.
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