a(HBP:"amyloid-beta oligomers") increases p(HGNC:MAPT, pmod(HBP:hyperphosphorylation))

PubMed:17403556

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).

Related Edges 3

• a(HBP:"amyloid-beta antibody, NU1") decreases complex(a(HBP:"amyloid-beta derived diffusible ligands"), a(MESH:Neurons))
• a(HBP:"amyloid-beta antibody, NU1") decreases p(HGNC:MAPT, pmod(Ph, Thr, 231))
• a(HBP:"amyloid-beta antibody, NU1") decreases complex(a(GO:synapse), a(HBP:"amyloid-beta derived diffusible ligands"))

MeSH

Alzheimer Disease

Text Location

Results

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