Vesicle permeabilization by protofibrillar alpha-synuclein: implications for the pathogenesis and treatment of Parkinson's disease.

By Michael J. Volles, Seung Jae Lee, J. Rochet, M. Shtilerman, T. T. Ding, Jeffrey C. Kessler, P. Lansbury. Biochemistry, 2001

709 citations recorded by the source corpus.

Subfields: Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/e0b34a65c7f5019f626f3644e0d384ce029a24b3

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Citations in the corpus

Alpha-synuclein, especially the Parkinson's disease-associated mutants, forms pore-like annular and tubular protofibrils. (2002, background): “The far-UV CD spectrum was consistent with a high content of b-sheet for the annular and tubular protofibrils.(19) The facts that the major protofibrillar species in this fraction is the 13 S species, and that the diameters of the annular and tubular protofibrils are very similar, suggest that the t”
Molecular mechanisms of neurodegeneration in Alzheimer's disease. (2010, background): “The primary pathogenic event triggering synaptic loss and selective neuronal cell death in these disorders is the subject of debate (51, 80), however recent studies suggest that nerve damage might result from the conversion of normally non-toxic monomers to toxic oligomers (34, 81-83) (Figure 2), wh”
Paradigm shifts in Alzheimer's disease and other neurodegenerative disorders: The emerging role of oligomeric assemblies (2002, neutral): “-synuclein assemblies (Volles et al., 2001).”
Secondary Structure of α-Synuclein Oligomers: Characterization by Raman and Atomic Force Microscopy (2006, background): “On the other hand, the Lansbury group, on the basis of far-UV CD studies, believes that spheroidal a-synuclein oligomers are rich in b-sheet structure and that the conversion from monomer to oligomers involves a secondary structural transition from natively unfolded to predominantly b-sheet.(9) Our ”
Parkinson's Disease Mechanisms and Models (2003, background): “…this view and the association of -synuclein with synaptic vesicles,presynaptic nerve terminals in close association with synaptic vesicles (Maroteaux et al., 1988; George et al., protofibrils may cause toxicity by permeabilizing synaptic vesicles (Volles et al., 2001; Lashuel et al., 2002),1995).”
Cell-Produced α-Synuclein Is Secreted in a Calcium-Dependent Manner by Exosomes and Impacts Neuronal Survival (2010, background): “…which greatly compromises membrane integrity, and lead to neuronal degeneration via the creation of significant alterations in the equilibrium of ions and small metabolites between the cytoplasm and the extracellular space (Heiser et al., 2000; Volles et al., 2001; Volles and Lansbury, 2003).”
DJ-1 Is a Redox-Dependent Molecular Chaperone That Inhibits α-Synuclein Aggregate Formation (2004, background): “Incubation of purified WT human aSyn for 2 h at 55 8C results in the generation of high molecular weight multimers that likely represent protofibrils (Figure 2A and 2B) (Volles et al. 2001; Gosavi et al. 2002).”
In vivo demonstration that α-synuclein oligomers are toxic (2011, result): “In agreement with previous reports, α-syn had a binding preference for anionic vesicles (29, 30).”