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Пленарное заседание ФОПФ и междисциплинарного центра фундаментальных исследований

опубликовано: 22.11.2013

27 ноября 2013 г. в 10:00 в 119 аудитории главного корпуса в рамках 56-й научной конференции МФТИ состоится пленарное заседание факультета общей и прикладной физики и междисциплинарного центра фундаментальных исследований:


Institut f?r Physikalische Biologie, Heinrich-Heine-Universit?t, D?sseldorf, Germany

Institute of Complex Systems, ICS-6: Structural Biochemistry, Research Centre J?lich, J?lich




Alzheimer’s disease (AD) is a progressive neurodegenerative disorder. Several lines of evidence suggest a central role of amyloid-B-peptide (AB) in the pathogenesis of AD. More than AB fibrils, small soluble and prion-like AB oligomers are suspected to be the major toxic species responsible for disease development and progression. Therefore, these oligomers should be our major target for therapy and used as the most direct biomarker for diagnosis and therapy monitoring. Diagnosis: The AB oligomer count in CSF of AD-affected and healthy persons as determined by our new ultra-sensitive surface-based fluorescence intensity distribution analysis (sFIDA) assay revealed a surprisingly clear distinction between both groups. All samples of the control group showed homogenously low numbers of AB oligomers, while the samples of the AD group exhibited significantly higher levels of AB oligomers with high variability. The AB oligomer levels clearly correlated with the patients’ mini-mental state examination (MMSE) scores. Therapy: We present our newest in vitro and in vivo results on D-enantiomeric peptide derivatives that specifically bind to Abeta oligomers and convert them into non-amyloidogenic, non-fibrilar and non-toxic species without increasing the concentration of monomeric AB. We show that next to plaque load and inflammation reduction, oral application of the peptide improved cognitive performance of AD transgenic mice.

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