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A role for b2* nicotinic receptors in a model of local amyloid pathology induced in dentate gyrus 1.0.0

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charles.hoyt@scai.fraunhofer.de at 2019-02-27 16:16:45.653335
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
21
Number Edges
40
Number Components
1
Network Density
0.0952380952380952
Average Degree
1.9047619047619
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
Role of the nicotinic acetylcholine receptor in Alzheimer's disease pathology and treatment v1.0.1 43%
Tau Modifications v1.9.5 38%
albuquerque2009 v1.0.0 38%
Nicotinic Receptor Abnormalities of Alzheimer’s Disease: Therapeutic Implications v1.0.0 33%
Amyloid β oligomers (AβOs) in Alzheimer’s disease v1.0.0 29%
Activation of M1 and M4 muscarinic receptors as potential treatments for Alzheimer's disease and schizophrenia. v1.0.0 29%
Selective activation of α7 nicotinic acetylcholine receptor by PHA-543613 improves Aβ25-35-mediated cognitive deficits in mice v1.0.0 27%
Chronic Anatabine Treatment Reduces Alzheimer ’ s Disease (AD)-Like Pathology and Improves Socio-Behavioral Deficits in a Transgenic Mouse Model of AD v1.0.0 25%
The Ubiquitin Proteasome System in Neurodegenerative Diseases: Sometimes the Chicken, Sometimes the Egg v1.0.0 24%
Clearance of Amyloid Beta and Tau in Alzheimer’s Disease:from Mechanisms to Therapy v1.0.1 24%

Sample Edges

complex(a(CHEBI:"amyloid-beta"), p(FPLX:CHRN)) hasComponent a(CHEBI:"amyloid-beta") View Subject | View Object

complex(a(CHEBI:"amyloid-beta"), p(FPLX:CHRN)) hasComponent p(FPLX:CHRN) View Subject | View Object

bp(GO:"inflammatory response") causesNoChange path(MESH:"Memory Disorders") View Subject | View Object

We did not detect any glia or microglia activation in WT-APP (Fig. 3C and F) compared with WT-GFP (Fig. 3B and E), meaning that the neuroinflammation does not play a role in the memory deficit we observed PubMed:27522251

Annotations
MeSH
Dentate Gyrus

bp(GO:aging) association p(MGI:Chrna7) View Subject | View Object

However, we identify a possible role of the alpha7 subunit in the normal aging process that should be further investigated PubMed:27522251

Annotations
MeSH
Dentate Gyrus

complex(a(CHEBI:"amyloid-beta"), p(FPLX:CHRN)) increases path(MESH:"Memory Disorders") View Subject | View Object

The hAPP-SLA transduction in DG did not induce a memory deficit in beta2 KO, meaning that the Abeta/beta2-nAChR interaction is required to drive the memory deficit in this model PubMed:27522251

Annotations
MeSH
Dentate Gyrus

Sample Nodes

a(CHEBI:"amyloid-beta")

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

bp(GO:"inflammatory response")

In-Edges: 55 | Out-Edges: 24 | Explore Neighborhood | Download JSON

bp(GO:aging)

In-Edges: 27 | Out-Edges: 61 | Explore Neighborhood | Download JSON

path(MESH:"Alzheimer Disease")

In-Edges: 536 | Out-Edges: 704 | Classes: 5 | Explore Neighborhood | Download JSON

bp(GO:"microglial cell activation")

In-Edges: 18 | Out-Edges: 8 | 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.