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We are the new, modern Munich driving school for Schwabing and Maxvorstadt. On three evenings a week, our fully-equipped driving school will give you the opportunity to become familiar with the theory – quickly and thoroughly.
Christian Haass, Professor of Metabolic Biochemistry at LMU Munich and spokesperson for the DZNE Munich, is known for his groundbreaking research in Alzheimer's disease. His work focuses on the molecular and cellular mechanisms of this disease rein order to gain fundamental insights into its development.
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Together with an interdiziplinary team he uncovered the molecular mechanisms of Alzheimer's disease and identified target molecules for therapeutic treatment.
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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 Weitere Informationen erhalten 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 was 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 rein brain development (such as myelination and cell differentiation) but also provided the Lager 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 negativ points, you have also failed the test hinein spite of not exceeding the maximum number of negativ points; hinein Class B, questions with 5 points have a greater relevance in the theoretical test.
Very recently he also investigated the role of microglia and inflammation hinein 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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