- EGCG remodels mature alpha-synuclein and amyloid-beta fibrils and reduces cellular toxicityJan Bieschke
Max Delbrueck Center for Molecular Medicine, Robert Roessle Strasse 10, 13125 Berlin Buch, Germany
Proc Natl Acad Sci U S A 107:7710-5. 2010..These findings suggest that EGCG is a potent remodeling agent of mature amyloid fibrils...
- Small-molecule conversion of toxic oligomers to nontoxic β-sheet-rich amyloid fibrilsJan Bieschke
Neuroproteomics, Max Delbrueck Center for Molecular Medicine, Berlin, Germany
Nat Chem Biol 8:93-101. 2012..These results support the hypothesis that small, diffusible prefibrillar amyloid species rather than mature fibrillar aggregates are toxic for mammalian cells...
- EGCG redirects amyloidogenic polypeptides into unstructured, off-pathway oligomersDagmar E Ehrnhoefer
Max Delbrueck Center for Molecular Medicine, AG Neuroproteomics, 13092 Berlin, Germany
Nat Struct Mol Biol 15:558-66. 2008..Instead of beta-sheet-rich amyloid, the formation of unstructured, nontoxic alpha-synuclein and amyloid-beta oligomers of a new type is promoted, suggesting a generic effect on aggregation pathways in neurodegenerative diseases...
- Black tea theaflavins inhibit formation of toxic amyloid-β and α-synuclein fibrilsGerlinde Grelle
Max Delbruck Centrum fur Molekulare Medizin, Robert Roessle Strasse 10, 13125 Berlin Buch, Germany
Biochemistry 50:10624-36. 2011..When compared to EGCG, TF3 was less susceptible to air oxidation and had an increased efficacy under oxidizing conditions. These findings suggest that theaflavins might be used to remove toxic amyloid deposits...
- Amyloid-β(1-42) Aggregation Initiates Its Cellular Uptake and CytotoxicitySha Jin
From the Proteomics and Molecular Mechanisms of Neurodegenerative Diseases, Max Delbruck Center for Molecular Medicine, 13125 Berlin Buch, Germany, The Department of Biomedical Engineering, Washington University, St Louis, Missouri 63130
J Biol Chem 291:19590-606. 2016..This process correlated with metabolic inhibition. Our data therefore imply that the formation of β-sheet-rich aggregates is a prerequisite for Aβ(1-42) uptake and cytotoxicity. ..