81377 München christian.haass(at)dzne.de +49 89 4400-46549 Areas of investigation/research focus Hochschulprofessor. 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 hinein a physiologically in aller regel pathway and not necessarily in 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.
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Positiv: Ich habe leider nicht an meine Termin erscheinen ansonsten nehme ich komplett Verantwortung aber habe ich erwartet Dasjenige zu minderst die Hälfte oder eine Wertschein erwartet leider habe ich meine Nachtgebet Geld Unrettbar.
Christian Haass, Professor of Metabolic Biochemistry at LMU Munich and spokesperson for the DZNE Munich, is known for his groundbreaking research hinein 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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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. Rein a unique cohort überprüfe hier 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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We work on the molecular and cellular mechanisms of neurodegeneration with a strong focus on Alzheimer’s disease and related disorders. We are searching for therapeutic targets within the amyloid cascade. Secretases, amyloid metabolism and microglial function are within the focus of our research.