Provenance

Upload
charles.hoyt@scai.fraunhofer.de at 2019-03-15 15:43:43.818554
Authors
Esther Wollert
Contact
charles.hoyt@scai.fraunhofer.de
License
CC BY 4.0
Copyright
Copyright © 2019 Fraunhofer Institute SCAI, All rights reserved.
Number Nodes
20
Number Edges
37
Number Components
1
Network Density
0.0973684210526316
Average Degree
1.85
Number Citations
1
Number BEL Errors
0

Content Statistics

Network Overlap

The node-based overlap between this network and other networks is calculated as the Szymkiewicz-Simpson coefficient of their respective nodes. Up to the top 10 are shown below.

Network Overlap
Phytochemicals as inhibitors of NF-κB for treatment of Alzheimer’s disease v1.0.0 35%
Upstream regulators and downstream effectors of NF-κBinAlzheimer's disease v1.0.0 35%
Nicotinic acetylcholine receptor signalling: roles in Alzheimer's disease and amyloid neuroprotection. v1.0.0 35%
Tau Modifications v1.9.5 35%
Caenorhabditis elegans models of tauopathy v1.0.0 25%
albuquerque2009 v1.0.0 25%
A role for b2* nicotinic receptors in a model of local amyloid pathology induced in dentate gyrus v1.0.0 25%
Anti-inflammatory activity of anatabine via inhibition of STAT3 phosphorylation v1.0.0 25%
Inflammasome Involvement in Alzheimer’s Disease v1.0.0 25%
Tau in physiology and pathology v1.0.0 20%

Sample Edges

a(CHEBI:"amyloid-beta") increases bp(GO:locomotion) View Subject | View Object

Transgenic mouse models of AD overexpressing Aβ peptides generally show greater locomotor activity and disinhibition in the elevated plus maze compared to non-transgenic mice, suggest- ing hyperactivity and a lower level of anxiety [28–30]. PubMed:26010758

Annotations
MeSH
Alzheimer Disease

a(CHEBI:"amyloid-beta") decreases path(MESH:Anxiety) View Subject | View Object

Transgenic mouse models of AD overexpressing Aβ peptides generally show greater locomotor activity and disinhibition in the elevated plus maze compared to non-transgenic mice, suggest- ing hyperactivity and a lower level of anxiety [28–30]. PubMed:26010758

Annotations
MeSH
Alzheimer Disease

a(CHEBI:"amyloid-beta") decreases path(MESH:"Interpersonal Relations") View Subject | View Object

Unlike wild-type mice, Tg PS1/APPswe mice elicited social interaction deficits and spent an equal amount of time in the chamber containing the empty cage or the chamber containing the unfamiliar (Stranger 1) mouse (Fig 4A). Anatabine at a dosage of 20mg/Kg/Day restored sociability in Tg PS1/APPswe mice as Tg PS1/APPswe mice treated with anatabine spent significantly more time in the chamber containing the unfamiliar mouse (Stranger 1) and less time in the chamber containing the empty cage (Fig 4B). PubMed:26010758

Annotations
MeSH
Alzheimer Disease

Sample Nodes

a(CHEBI:"amyloid-beta")

In-Edges: 423 | Out-Edges: 245 | Children: 5 | Explore Neighborhood | Download JSON

p(HGNC:MAPT)

In-Edges: 477 | Out-Edges: 480 | Classes: 11 | Children: 27 | Explore Neighborhood | Download JSON

p(HGNC:MAPT, pmod(Ph))

In-Edges: 201 | Out-Edges: 71 | Classes: 1 | Children: 4 | Explore Neighborhood | Download JSON

About

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.