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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 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 Beryllium 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 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 in generation and liberation of the peptide and finally the development of selective inhibitors to therapeutically lower Aß production hinein patients.
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 hinein order to gain fundamental insights into its development.
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Is it possible for a good driving student to register for the test after having lessons only rein special driving situations? No, that is not possible because of the legal regulations.
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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 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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