81377  München christian.haass(at)dzne.de +49 89 4400-46549 Areas of investigation/research focus Professor. Haass started to work on Alzheimer's disease (AD) hinein 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 rein 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 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 hinein patients.

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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 team he uncov­ered the molec­u­lar mecha­nisms of Alzheimer's disease and identi­fied target molecules for thera­peu­tic treatment.

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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 Weitere Informationen erhalten 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 in the identification of TREM2 as a CSF marker for microglial activity.  Rein a unique cohort 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 ur research.