Small Molecule Inhibitors of Aggregation Indicate That Amyloid β Oligomerization and Fibrillization Pathways Are Independent and Distinct*
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R. Kayed | C. Glabe | S. Milton | Charles G. Glabe | Rakez Kayed | Mihaela Necula | Saskia Milton | M. Necula | Mihaela Necula
[1] R. Hepler,et al. Solution State Characterization of Amyloid β-Derived Diffusible Ligands , 2006 .
[2] Yun-Ru Chen,et al. Distinct Early Folding and Aggregation Properties of Alzheimer Amyloid-β Peptides Aβ40 and Aβ42 , 2006, Journal of Biological Chemistry.
[3] C. Glabe. Common mechanisms of amyloid oligomer pathogenesis in degenerative disease , 2006, Neurobiology of Aging.
[4] M. Gallagher,et al. A specific amyloid-β protein assembly in the brain impairs memory , 2006, Nature.
[5] Roland Winter,et al. Solvation-assisted pressure tuning of insulin fibrillation: from novel aggregation pathways to biotechnological applications. , 2006, Journal of molecular biology.
[6] W. Klein,et al. Temporal Profile of Amyloid-β (Aβ) Oligomerization in an in Vivo Model of Alzheimer Disease , 2006, Journal of Biological Chemistry.
[7] V. Uversky,et al. Early Events in the Fibrillation of Monomeric Insulin* , 2005, Journal of Biological Chemistry.
[8] R. V. van Breemen,et al. Mass spectrometry-based screening for inhibitors of beta-amyloid protein aggregation. , 2005, Analytical chemistry.
[9] A. Fink,et al. Characterization of Oligomeric Intermediates in α-Synuclein Fibrillation: FRET Studies of Y125W/Y133F/Y136F α-Synuclein , 2005 .
[10] L. Juliano,et al. Controlling {beta}-amyloid oligomerization by the use of naphthalene sulfonates: trapping low molecular weight oligomeric species. , 2005, The Journal of biological chemistry.
[11] S. Radford,et al. Competing pathways determine fibril morphology in the self-assembly of beta2-microglobulin into amyloid. , 2005, Journal of molecular biology.
[12] R. Sabaté,et al. Stimulatory and inhibitory effects of alkyl bromide surfactants on beta-amyloid fibrillogenesis. , 2005, Langmuir : the ACS journal of surfaces and colloids.
[13] C. Chirita,et al. Cyanine dye N744 inhibits tau fibrillization by blocking filament extension: implications for the treatment of tauopathic neurodegenerative diseases. , 2005, Biochemistry.
[14] David T. Kaleta,et al. Structural properties of Abeta protofibrils stabilized by a small molecule. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[15] Ian Parker,et al. Calcium Dysregulation and Membrane Disruption as a Ubiquitous Neurotoxic Mechanism of Soluble Amyloid Oligomers*♦ , 2005, Journal of Biological Chemistry.
[16] C. Chirita,et al. Triggers of full-length tau aggregation: a role for partially folded intermediates. , 2005, Biochemistry.
[17] Takeshi Iwatsubo,et al. Inhibition of Heparin-induced Tau Filament Formation by Phenothiazines, Polyphenols, and Porphyrins* , 2005, Journal of Biological Chemistry.
[18] R. Sabaté,et al. Temperature dependence of the nucleation constant rate in beta amyloid fibrillogenesis. , 2005, International journal of biological macromolecules.
[19] Fusheng Yang,et al. Curcumin Inhibits Formation of Amyloid β Oligomers and Fibrils, Binds Plaques, and Reduces Amyloid in Vivo* , 2005, Journal of Biological Chemistry.
[20] K. Nilsson,et al. Conjugated polyelectrolytes: conformation-sensitive optical probes for detection of amyloid fibril formation. , 2005, Biochemistry.
[21] G. Bloom,et al. Cultured cell and transgenic mouse models for tau pathology linked to β-amyloid , 2005 .
[22] K. Ono,et al. Anti-amyloidogenic activity of tannic acid and its activity to destabilize Alzheimer's beta-amyloid fibrils in vitro. , 2004, Biochimica et biophysica acta.
[23] Ehud Gazit,et al. Inhibition of islet amyloid polypeptide fibril formation: a potential role for heteroaromatic interactions. , 2004, Biochemistry.
[24] Walraj S. Gosal,et al. Fibrillar β-Lactoglobulin Gels: Part 1. Fibril Formation and Structure , 2004 .
[25] C. Glabe. Conformation-dependent antibodies target diseases of protein misfolding. , 2004, Trends in biochemical sciences.
[26] J. D. Figueroa-Villar,et al. Targeting the neurotoxic species in Alzheimer's disease: inhibitors of Aβ oligomerization , 2004, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[27] M. P. Kirpichnikov,et al. Fibrillation of carrier protein albebetin and its biologically active constructs. Multiple oligomeric intermediates and pathways. , 2004, Biochemistry.
[28] Shubo Han,et al. The Flavonoid Baicalein Inhibits Fibrillation of α-Synuclein and Disaggregates Existing Fibrils* , 2004, Journal of Biological Chemistry.
[29] J. Kuret,et al. Electron microscopy as a quantitative method for investigating tau fibrillization. , 2004, Analytical biochemistry.
[30] Peter Chien,et al. Emerging principles of conformation-based prion inheritance. , 2004, Annual review of biochemistry.
[31] Jie Li,et al. Dopamine and L‐dopa disaggregate amyloid fibrils: implications for Parkinson's and Alzheimer's disease , 2004, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[32] Joleen T White,et al. Transthyretin aggregation under partially denaturing conditions is a downhill polymerization. , 2004, Biochemistry.
[33] V. Uversky,et al. Stimulation of Insulin Fibrillation by Urea-induced Intermediates* , 2004, Journal of Biological Chemistry.
[34] U. Aebi,et al. Human Amylin Oligomer Growth and Fibril Elongation Define Two Distinct Phases in Amyloid Formation* , 2004, Journal of Biological Chemistry.
[35] Kenjiro Ono,et al. Curcumin has potent anti‐amyloidogenic effects for Alzheimer's β‐amyloid fibrils in vitro , 2004, Journal of neuroscience research.
[36] C. Chirita,et al. Ligand-dependent inhibition and reversal of tau filament formation. , 2004, Biochemistry.
[37] C. Chirita,et al. Evidence for an intermediate in tau filament formation. , 2004, Biochemistry.
[38] C. Dobson. Protein folding and misfolding , 2003, Nature.
[39] C. Finch,et al. Self-assembly of Aβ1-42 into globular neurotoxins , 2003 .
[40] V. Uversky,et al. Structural transformations of oligomeric intermediates in the fibrillation of the immunoglobulin light chain LEN. , 2003, Biochemistry.
[41] M. D'Andrea,et al. The use of formic acid to embellish amyloid plaque detection in Alzheimer's disease tissues misguides key observations , 2003, Neuroscience Letters.
[42] L. Fieser. 1,2‐Naphthoquinone , 2003 .
[43] Carl W. Cotman,et al. Common Structure of Soluble Amyloid Oligomers Implies Common Mechanism of Pathogenesis , 2003, Science.
[44] M. Manning,et al. Congo Red Populates Partially Unfolded States of an Amyloidogenic Protein to Enhance Aggregation and Amyloid Fibril Formation* , 2003, The Journal of Biological Chemistry.
[45] P. Fraser,et al. Alternate Aggregation Pathways of the Alzheimer β-Amyloid Peptide: Aβ Association Kinetics at Endosomal pH , 2003 .
[46] G. Damaschun,et al. Assembly of amyloid protofibrils via critical oligomers--a novel pathway of amyloid formation. , 2003, Journal of molecular biology.
[47] H. Lashuel,et al. New class of inhibitors of amyloid-beta fibril formation. Implications for the mechanism of pathogenesis in Alzheimer's disease. , 2002, The Journal of biological chemistry.
[48] Christopher A. Ross,et al. Huntingtin Spheroids and Protofibrils as Precursors in Polyglutamine Fibrilization* , 2002, The Journal of Biological Chemistry.
[49] C. Dobson,et al. Stimulation and inhibition of fibril formation by a peptide in the presence of different concentrations of SDS , 2002, FEBS letters.
[50] P. Lansbury,et al. Protofibrillar islet amyloid polypeptide permeabilizes synthetic vesicles by a pore-like mechanism that may be relevant to type II diabetes. , 2002, Biochemistry.
[51] Lei Chang,et al. Per-6-substituted β-cyclodextrin libraries inhibit formation of β-amyloid-peptide (Aβ)-derived, soluble oligomers , 2002, Journal of Molecular Neuroscience.
[52] F. Cohen,et al. Pathway Complexity of Prion Protein Assembly into Amyloid* , 2002, The Journal of Biological Chemistry.
[53] V. Uversky,et al. Elucidation of the Molecular Mechanism during the Early Events in Immunoglobulin Light Chain Amyloid Fibrillation , 2002, The Journal of Biological Chemistry.
[54] C. Dobson,et al. Inherent toxicity of aggregates implies a common mechanism for protein misfolding diseases , 2002, Nature.
[55] A. Miranker,et al. Islet amyloid: phase partitioning and secondary nucleation are central to the mechanism of fibrillogenesis. , 2002, Biochemistry.
[56] W. Klunk,et al. Inhibition of Polyglutamine Aggregation in R6/2 HD Brain Slices—Complex Dose–Response Profiles , 2001, Neurobiology of Disease.
[57] Peter T. Lansbury,et al. Kinetic Stabilization of the α-Synuclein Protofibril by a Dopamine-α-Synuclein Adduct , 2001, Science.
[58] M. Kirkitadze,et al. Identification and characterization of key kinetic intermediates in amyloid beta-protein fibrillogenesis. , 2001, Journal of molecular biology.
[59] W. Klunk,et al. Uncharged thioflavin-T derivatives bind to amyloid-beta protein with high affinity and readily enter the brain. , 2001, Life sciences.
[60] V. Papadopoulos,et al. The Ginkgo biloba extract EGb 761 rescues the PC12 neuronal cells from β-amyloid-induced cell death by inhibiting the formation of β-amyloid-derived diffusible neurotoxic ligands , 2001, Brain Research.
[61] Bin Zhang,et al. In vivo detection of amyloid plaques in a mouse model of Alzheimer's disease. , 2000 .
[62] H. Lehrach,et al. Inhibition of huntingtin fibrillogenesis by specific antibodies and small molecules: implications for Huntington's disease therapy. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[63] J. Dubochet,et al. Self-assembly of beta-amyloid 42 is retarded by small molecular ligands at the stage of structural intermediates. , 2000, Journal of structural biology.
[64] M. Davies,et al. In-situ atomic force microscopy study of beta-amyloid fibrillization. , 2000, Journal of molecular biology.
[65] J. Kemp,et al. Controlling Polymerization of β-Amyloid and Prion-derived Peptides with Synthetic Small Molecule Ligands* , 2000, The Journal of Biological Chemistry.
[66] D. Selkoe,et al. Amyloid beta-protein fibrillogenesis. Structure and biological activity of protofibrillar intermediates. , 1999, The Journal of biological chemistry.
[67] C. Dobson. Protein misfolding, evolution and disease. , 1999, Trends in biochemical sciences.
[68] Peter T. Lansbury,et al. Assembly of Aβ Amyloid Protofibrils: An in Vitro Model for a Possible Early Event in Alzheimer's Disease† , 1999 .
[69] Nybo,et al. An Ultrastructural Study of Amyloid Intermediates in Aβ1–42 Fibrillogenesis , 1999, Scandinavian journal of immunology.
[70] F. Gejyo,et al. Apolipoprotein E and antioxidants have different mechanisms of inhibiting Alzheimer's beta-amyloid fibril formation in vitro. , 1998, Biochemistry.
[71] George B. Benedek,et al. Temperature dependence of amyloid β-protein fibrillization , 1998 .
[72] T. Morgan,et al. Diffusible, nonfibrillar ligands derived from Abeta1-42 are potent central nervous system neurotoxins. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[73] R. Majocha,et al. Indomethacin Reverses the Microglial Response to Amyloid β-Protein , 1998, Neurobiology of Aging.
[74] C. Soto,et al. Inhibition of Alzheimer β-Fibrillogenesis by Melatonin* , 1998, The Journal of Biological Chemistry.
[75] D. Selkoe,et al. Oligomerization of endogenous and synthetic amyloid beta-protein at nanomolar levels in cell culture and stabilization of monomer by Congo red. , 1998, Biochemistry.
[76] P. Lansbury,et al. Atomic force microscopic imaging of seeded fibril formation and fibril branching by the Alzheimer's disease amyloid-beta protein. , 1997, Chemistry & biology.
[77] P. Cutler,et al. Hemin and related porphyrins inhibit β‐amyloid aggregation , 1997 .
[78] D. Walsh,et al. Amyloid beta-protein fibrillogenesis. Detection of a protofibrillar intermediate. , 1997, The Journal of biological chemistry.
[79] George B. Benedek,et al. Kinetic theory of fibrillogenesis of amyloid β-protein , 1997 .
[80] B. Seilheimer,et al. The toxicity of the Alzheimer's beta-amyloid peptide correlates with a distinct fiber morphology. , 1997, Journal of structural biology.
[81] S. Asano,et al. Inhibition of Amyloid Protein Aggregation and Neurotoxicity by Rifampicin , 1996, The Journal of Biological Chemistry.
[82] M. Hurle,et al. Selective Inhibition of A Fibril Formation , 1996, The Journal of Biological Chemistry.
[83] D. Kirschner,et al. On the nucleation and growth of amyloid beta-protein fibrils: detection of nuclei and quantitation of rate constants. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[84] H. Naiki,et al. First-order kinetic model of Alzheimer's beta-amyloid fibril extension in vitro. , 1996, Laboratory investigation; a journal of technical methods and pathology.
[85] S. Pollack,et al. Sulfonated dyes attenuate the toxic effects of β-amyloid in a structure-specific fashion , 1995, Neuroscience Letters.
[86] R. Wetzel,et al. Aggregation state and neurotoxic properties of Alzheimer beta-amyloid peptide. , 1995, Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration.
[87] P. Lansbury,et al. Apolipoprotein E is a kinetic but not a thermodynamic inhibitor of amyloid formation: implications for the pathogenesis and treatment of Alzheimer disease. , 1995, Proceedings of the National Academy of Sciences of the United States of America.
[88] B. Yankner,et al. Beta-amyloid neurotoxicity requires fibril formation and is inhibited by congo red. , 1994, Proceedings of the National Academy of Sciences of the United States of America.
[89] C. Glabe,et al. Surfactant properties of Alzheimer's A beta peptides and the mechanism of amyloid aggregation. , 1994, The Journal of biological chemistry.
[90] H. Mori,et al. Rifampicin prevents the aggregation and neurotoxicity of amyloid beta protein in vitro. , 1994, Biochemical and biophysical research communications.
[91] P. Camilleri,et al. β‐Cyclodextrin interacts with the Alzheimer amyloid β‐A4 peptide , 1994 .
[92] Carl W. Cotman,et al. Neurodegeneration induced by beta-amyloid peptides in vitro: the role of peptide assembly state , 1993, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[93] H. Levine,et al. Thioflavine T interaction with synthetic Alzheimer's disease β‐amyloid peptides: Detection of amyloid aggregation in solution , 1993, Protein science : a publication of the Protein Society.
[94] C. Cotman,et al. Assembly and aggregation properties of synthetic Alzheimer's A4/beta amyloid peptide analogs. , 1992, The Journal of biological chemistry.
[95] Carl W. Cotman,et al. In vitro aging of ß-amyloid protein causes peptide aggregation and neurotoxicity , 1991, Brain Research.
[96] D. Selkoe. The molecular pathology of Alzheimer's disease , 1991, Neuron.
[97] J. Pettegrew,et al. Quantitative evaluation of congo red binding to amyloid-like proteins with a beta-pleated sheet conformation. , 1989, The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society.
[98] E. O. Schlemper. 2,2'-Dihydroxybenzophenone , 1982 .
[99] J. Hardy,et al. The Amyloid Hypothesis of Alzheimer ’ s Disease : Progress and Problems on the Road to Therapeutics , 2009 .
[100] C. Glabe. Amyloid accumulation and pathogensis of Alzheimer's disease: significance of monomeric, oligomeric and fibrillar Abeta. , 2005, Sub-cellular biochemistry.
[101] Peter T. Lansbury,et al. Observation of metastable Aβ amyloid protofibrils by atomic force microscopy , 1997 .
[102] P. Lansbury,et al. Models of amyloid seeding in Alzheimer's disease and scrapie: mechanistic truths and physiological consequences of the time-dependent solubility of amyloid proteins. , 1997, Annual review of biochemistry.