Chris­t­ian Haass is a German Biochemist and known for his work on the cell biology of neurode­gen­er­a­tive diseases.

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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 was 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 in brain development (such as myelination and cell differentiation) but also provided the Stützpunkt for several current therapeutic approaches.

Positiv: Ich habe leider nicht an meine Termin erscheinen des weiteren nehme ich komplett Verantwortung aber habe ich erwartet Dasjenige nach minderst die Hälfte oder eine Wertschein erwartet leider habe ich meine Komplet Währungs Unrettbar.

Haass welches awarded the Hector Science Award and is currently leading a major project on the clini­cal testing of an Alzheimer's antibody.

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The theoretical test must be passed within one year of registering for a driving licence; hier klicken hinein this period you can take the test as often as you wish. After failing the test twice, however, you must observe a three-month waiting period. The respective Elfe for the test must be paid each time.

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  Very recently he also investigated the role of microglia and inflammation hinein neurodegenerative disorders.  This work Lumineszenzdiode to the spectacular finding that microglial phagocytosis may be 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 was 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.

We are using interdisciplinary approaches ranging from biophysics, biochemistry and cellular and molecular biology to rein vivo models and life imaging.

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