Details, Fiktion und Motorradführerschein Kaiserslautern
Details, Fiktion und Motorradführerschein Kaiserslautern
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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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Together with an interdiziplinary Mannschaft he uncovered the molecular mechanisms of Alzheimer's disease and identified target molecules for therapeutic treatment.
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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) in 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 in this field that Aß may be produced from its precursor in a physiologically gewöhnlich 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 hinein generation and liberation of the peptide and finally the development of selective inhibitors to therapeutically lower Aß production in 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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Very recently he also investigated the role of microglia and inflammation in 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 rein the identification of TREM2 as a CSF marker for microglial activity. Rein 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.
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