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complex(a(HBP:"amyloid-beta derived diffusible ligands"), a(MESH:Neurons))

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Alzheimer's disease-type neuronal tau hyperphosphorylation induced by A beta oligomers v1.0.0

This document contains the bel code for the Article Alzheimer’s disease-type neuronal tau hyperphosphorylation induced by Abeta oligomers by De Felice et al

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a(HBP:"amyloid-beta antibody, NU1") decreases complex(a(HBP:"amyloid-beta derived diffusible ligands"), a(MESH:Neurons)) View Subject | View Object

Moreover, the presence of large extracellular aggregates in NU1-treated cultures (Fig. 5N) suggests that the antibody effectively sequesters ADDLs and prevents their interactions with neurons (Fig. 5O). No inhibition of ADDL binding was associated with PP1 and LY294002 (Fig. 5H, I, K and L, respectively), but both kinase inhibitors effectively blocked ADDL-induced tau hyperphosphorylation (Fig. 5G and J). PubMed:17403556

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a(HBP:"amyloid-beta antibody, NU1") decreases complex(a(HBP:"amyloid-beta derived diffusible ligands"), a(MESH:Neurons)) View Subject | View Object

Importantly, pre-incubation of AD brain extracts with NU1 significantly blocked the increase in Thr231 phosphotau immunofluorescence (Fig. 6G), establishing the tau hyperphosphorylation was induced by Abeta oligomers in the AD brain extracts. NU1 also prevented the binding of brain-derived ADDLs to synaptic hot-spots (Fig. 6H and I). In NU1-treated cultures, the presence of large extracellular aggregates indicates that the antibody sequesters ADDLs and prevents their interactions with neurons (Fig. 6I). PubMed:17403556

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Alzheimer Disease
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complex(a(HBP:"amyloid-beta derived diffusible ligands"), a(MESH:Neurons)) hasComponent a(HBP:"amyloid-beta derived diffusible ligands") View Subject | View Object

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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.