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- W2125530178 abstract "Microtubule-based neuronal transport pathways are impaired during the progression of Alzheimer's disease and other neurodegenerative conditions. However, mechanisms leading to defects in transport remain to be determined. We quantified morphological changes in neuronal cells following treatment with fibrils and unaggregated peptides of beta-amyloid (Aβ). Aβ fibrils induce axonal and dendritic swellings indicative of impaired transport. In contrast, Aβ peptides induce a necrotic phenotype in both neurons and non-neuronal cells. We tested several popular hypotheses by which aggregated Aβ could disrupt transport. Using fluorescent polystyrene beads, we developed experimental models of physical blockage and localized release of reactive oxygen species (ROS) that reliably induce swellings. Like the beads, Aβ fibrils localize in close proximity to swellings; however, fibril internalization is not required for disrupting transport. ROS and membrane permeability are also unlikely to be responsible for fibril-mediated toxicity. Collectively, our results indicate that multiple initiating factors converge upon pathways of defective transport." @default.
- W2125530178 created "2016-06-24" @default.
- W2125530178 creator A5018920244 @default.
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- W2125530178 creator A5077553890 @default.
- W2125530178 creator A5079367953 @default.
- W2125530178 creator A5082111878 @default.
- W2125530178 date "2009-10-01" @default.
- W2125530178 modified "2023-10-15" @default.
- W2125530178 title "Examination of potential mechanisms of amyloid-induced defects in neuronal transport" @default.
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