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Adenosine A1 receptor antagonist 64627 alleviates axonopathy caused by human Tau ΔK280 1.0.0

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charles.hoyt@scai.fraunhofer.de at 2019-02-27 16:23:05.969692
Authors
Sandra Spalek
Contact
charles.hoyt@scai.fraunhofer.de
License
CC BY 4.0
Copyright
Copyright © 2018 Fraunhofer Institute SCAI, All rights reserved.
Number Nodes
45
Number Edges
104
Number Components
1
Network Density
0.0525252525252525
Average Degree
2.31111111111111
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
Anti-aggregant tau mutant promotes neurogenesis v1.0.0 30%
Tau Modifications v1.9.5 24%
Tau Antibody Targeting Pathological Species Blocks Neuronal Uptake and Interneuron Propagation of Tau in Vitro v1.0.0 18%
The Ubiquitin–Proteasome System and the Autophagic–Lysosomal System in Alzheimer Disease v1.0.0 16%
Extracellular low-n oligomers of tau cause selective synaptotoxicity without affecting cell viability v1.0.0 14%
Alzheimer’s disease and the autophagic-lysosomal system v1.0.0 13%
mTOR-Related Brain Dysfunctions in Neuropsychiatric Disorders v1.0.0 13%
Role of the nicotinic acetylcholine receptor in Alzheimer's disease pathology and treatment v1.0.1 13%
Tau clearance mechanisms and their possible role in the pathogenesis of Alzheimer disease v1.0.0 13%
Inert and seed-competent tau monomers suggest structural origins of aggregation v1.0.0 12%

Sample Edges

a(CHEBI:ATP) positiveCorrelation a(GO:mitochondrion) View Subject | View Object

ATP is reduced in the proaggregant transgenic slices, matching the lower mitochondrial density, compared with littermate controls or antiaggregant Tau transgenic slices (Fig. 3H) PubMed:27671637

a(CHEBI:adenosine) increases act(p(MGI:Adora1)) View Subject | View Object

Adenosine downmodulates neuronal activity (cFos levels), impairs the presynapse, and attenuates long-term potentiation (LTP) via the A1 receptor (21) PubMed:27671637

a(CHEBI:adenosine) decreases act(a(MESH:Neurons)) View Subject | View Object

Adenosine downmodulates neuronal activity (cFos levels), impairs the presynapse, and attenuates long-term potentiation (LTP) via the A1 receptor (21) PubMed:27671637

a(CHEBI:adenosine) decreases act(a(GO:presynapse)) View Subject | View Object

Adenosine downmodulates neuronal activity (cFos levels), impairs the presynapse, and attenuates long-term potentiation (LTP) via the A1 receptor (21) PubMed:27671637

a(CHEBI:adenosine) decreases bp(GO:"long-term synaptic potentiation") View Subject | View Object

Adenosine downmodulates neuronal activity (cFos levels), impairs the presynapse, and attenuates long-term potentiation (LTP) via the A1 receptor (21) PubMed:27671637

Sample Nodes

bp(GO:"response to oxidative stress")

In-Edges: 15 | Out-Edges: 12 | Explore Neighborhood | Download JSON

a(GO:"neurofibrillary tangle")

In-Edges: 74 | Out-Edges: 61 | Children: 1 | Explore Neighborhood | Download JSON

bp(GO:"astrocyte activation")

In-Edges: 7 | Out-Edges: 6 | Explore Neighborhood | Download JSON

bp(GO:"long-term synaptic potentiation")

In-Edges: 39 | Out-Edges: 20 | Explore Neighborhood | Download JSON

a(MESH:Neurons)

In-Edges: 50 | Out-Edges: 16 | 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.