EINE UNVOREINGENOMMENE SICHT AUF FAHRSCHULE

Eine unvoreingenommene Sicht auf fahrschule

Eine unvoreingenommene Sicht auf fahrschule

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

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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 welches 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 rein this field that Aß may be produced from its precursor in a physiologically üblich pathway and not necessarily rein 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 in generation and liberation of the peptide and finally the development of selective inhibitors to therapeutically lower Aß production rein patients.

Chris­t­ian Haass, Profes­sor Weitere Informationen erhalten 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 hinein order to gain funda­men­tal insights into its devel­op­ment.

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  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.  Hinein 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 in vivo models and life imaging.

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