Protofibrils, pores, fibrils, and neurodegeneration: separating the responsible protein aggregates from the innocent bystanders.

By B. Caughey, P. Lansbury. Annual Review of Neuroscience, 2003

1,735 citations recorded by the source corpus.

Subfields: Molecular Biology, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/aada252aa202858159e05834c4398f75b1ae1d66

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Citations in the corpus

Experimental constraints on quaternary structure in Alzheimer's beta-amyloid fibrils. (2006, background): “The data include: (1) two-dimensional 13C-13C NMR spectra that indicate internal quaternary contacts between sidechains of L17 and F19 and sidechains of I32, L34, and V36, as well as external quaternary contacts between sidechains of I31 and G37; (2) two-dimensional 15N-13C NMR spectra that indicate”
Modulation of neurodegeneration by molecular chaperones (2005, methodology): “ATOMIC FORCE MICROSCOPY (AFM) of the aggregation of amyloid-β (Aβ) and α-synuclein proteins has been used to characterize several metastable structures, such as SPHERICAL OLIGOMERS , protofibrils and pore-like ANNULAR structures, which might be components of a pathway to fibril formatio”
In vivo demonstration that α-synuclein oligomers are toxic (2011, background): “These oligomers interact with lipids, disrupt membranes (7, 8), and cause cell death in vitro (10, 11) and in nonmammalian models, such as Caenorhabditis elegans and Drosophila melanogaster (12).”
Protein folding and misfolding (2003, background): “Experiments in vitro indicate that their formation is then generally characterized by a lag phase, followed by a period of rapid growt”
TDP-43 and FUS/TLS: emerging roles in RNA processing and neurodegeneration. (2010, background): “As in most neurodegenerative diseases where cytoplasmic aggregations are evident, an unresolved controversy is whether inclusions are neurotoxic or neuroprotective (232), the latter presumably through the sequestration of smaller toxic species of misfolded proteins.”
Involvement of Oxidative Stress in Alzheimer Disease (2006, background): “An increasing body of evidence has been collected to support the hypothesis that oligomers, not monomers or fibrils, are the toxic fraction of the protein (reviewed in [90, 91]).”
Expanding insights of mitochondrial dysfunction in Parkinson's disease (2006, background): “However, controversy remains about which species is the toxic culpri”