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Appears in Networks 5

In-Edges 9

p(HGNC:APP, frag("672_713")) increases a(HBP:HBP00022) View Subject | View Object

Studies done on familial AD (FAD) mutations consistently show increases in the ratio of Abeta42/40 [105,144], suggesting that elevated levels of Abeta42 relative to Abeta40 is critical for AD pathogenesis, probably by providing the core for Abeta assembly into oligomers, fibrils and amyloidogenic plaques [145,146] PubMed:21214928

Annotations
MeSH
Endosomes
Confidence
High
MeSH
Neurons

p(HGNC:APP, frag("672_713")) increases a(HBP:HBP00022) View Subject | View Object

Studies also suggest that increased Abeta 42 levels probably provide the core for oligomerization, fibrillation and amyloid plaque generation (Jarrett et al. 1993; Iwatsubo et al. 1994) PubMed:22122372

composite(p(MGI:App, var("p.Lys670Asn"), var("p.Met671Leu"), var("p.Thr714Ile"), var("p.Val717Ile")), p(MGI:Chrna7)) decreases a(HBP:HBP00022) View Subject | View Object

Immunofluorescence performed with VHH 31-1 on brain slices of APP-alpha7 mice also showed intracellular Abeta oligomers in the polymorphic layer (Fig. 8, arrows), whereas GFP-alpha7 mice did not show any Abeta oligomers PubMed:27522251

p(MGI:App, var("p.Lys670Asn"), var("p.Met671Leu"), var("p.Thr714Ile"), var("p.Val717Ile")) increases a(HBP:HBP00022) View Subject | View Object

The presence of oligomeric Abeta in APP-WT was confirmed with the antibody VHH 31-1, specific for oligomeric forms of Abeta (Lafaye et al., 2009) PubMed:27522251

p(MGI:App, var("p.Lys670Asn"), var("p.Met671Leu"), var("p.Thr714Ile"), var("p.Val717Ile")) increases a(HBP:HBP00022) View Subject | View Object

Abeta intracellular accumulation in DG polymorphic layer was also confirmed with the rat monoclonal 7H3D6 antibody, also specific for oligomeric Abeta (Kumar et al., 2013) (Fig. 7, arrow) PubMed:27522251

p(MGI:Chrna7) increases a(HBP:HBP00022) View Subject | View Object

Immunofluorescence performed with VHH 31-1 on brain slices of APP-alpha7 mice also showed intracellular Abeta oligomers in the polymorphic layer (Fig. 8, arrows), whereas GFP-alpha7 mice did not show any Abeta oligomers PubMed:27522251

composite(p(MGI:App, var("p.Lys670Asn"), var("p.Met671Leu"), var("p.Thr714Ile"), var("p.Val717Ile")), p(MGI:Chrnb2)) decreases a(HBP:HBP00022) View Subject | View Object

We then investigated the presence of Abeta aggregates in the hippocampus of APP-beta2 and APP-alpha7. In APP-beta2, a positive staining for Abeta oligomers using the VHH 31-1 antibody was found (Fig. 8, arrows) PubMed:27522251

a(CHEBI:curcumin) decreases a(HBP:HBP00022) View Subject | View Object

Pro-autophagic effects of curcumin are reflected in improved function in cellular and animal models of PD and AD, as well as reduced levels of α-synuclein aggregates 144 or Aβ and tau oligomers 145,146 . PubMed:30116051

Out-Edges 2

a(HBP:HBP00022) decreases bp(GO:"synaptic signaling") View Subject | View Object

It has been postulated that soluble or small oligomeric forms of Ab have deleterious effects in the brain, inducing impaired synaptic function and promoting neuronal degeneration [5]. PubMed:21718217

a(HBP:HBP00022) increases bp(GO:"neuron death") View Subject | View Object

It has been postulated that soluble or small oligomeric forms of Ab have deleterious effects in the brain, inducing impaired synaptic function and promoting neuronal degeneration [5]. PubMed:21718217

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BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

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.