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Inflammasome Involvement in Alzheimer’s Disease 1.0.0

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charles.hoyt@scai.fraunhofer.de at 2019-02-27 16:23:52.387478
Authors
Esther Wollert
Contact
charles.hoyt@scai.fraunhofer.de
License
CC BY 4.0
Copyright
Copyright © 2018 Fraunhofer Institute SCAI, All rights reserved.
Number Nodes
46
Number Edges
88
Number Components
2
Network Density
0.042512077294686
Average Degree
1.91304347826087
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
Estrogen receptor-α is localized to neurofibrillary tangles in Alzheimer's disease v1.0.0 50%
Tau Modifications v1.9.5 33%
Nuclear Factor Kappa-light-chain-enhancer of Activated B Cells (NF-κB) - a Friend, a Foe, or a Bystander - in the Neurodegenerative Cascade and Pathogenesis of Alzheimer's Disease v1.0.0 30%
Activation and regulation of the inflammasomes v1.0.0 30%
Inflammasome activation and innate immunity in Alzheimer’s disease v1.0.2 29%
Phytochemicals as inhibitors of NF-κB for treatment of Alzheimer’s disease v1.0.0 28%
The role of inflammasome in Alzheimer’s disease v1.0.3 26%
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%
Inert and seed-competent tau monomers suggest structural origins of aggregation v1.0.0 25%
Alzheimer’s disease and the autophagic-lysosomal system v1.0.0 24%

Sample Edges

p(HGNC:MAPT) hasVariant p(HGNC:MAPT, pmod(Ph)) View Subject | View Object

a(CHEBI:"RNA fragment") increases act(complex(GO:"NLRP3 inflammasome complex")) View Subject | View Object

Of these, the NLRP3 inflammasome can be acti- vated via bacterial RNA species [3]. PubMed:27314526

Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph

a(CHEBI:"amyloid-beta") association p(HGNC:NLRP3) View Subject | View Object

In AD, microglial cells and astrocytes express NLRP3, which in turn can detect A beta plaques and act by secreting caspase-1 to activate IL-1 beta and IL- 18 [23–25]. PubMed:27314526

Annotations
Confidence
Medium
MeSH
Alzheimer Disease
NeuroMMSigDB
Amyloidogenic subgraph
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

a(CHEBI:"nitric oxide") increases a(CHEBI:peroxynitrite) View Subject | View Object

It is noteworthy that IL-1 beta and IL-18 can activate various cell types, par- ticularly astrocytes and microglia to induce additional cytokine release involving IL-1 beta , IL-6, and IL-18, and also nitric oxide (NO) synthase that can stimulate production of free radical NO, leading to the forma- tion of peroxynitrite that denatures DNA and impairs cellular energy pathways [48, 49]. PubMed:27314526

Annotations
Confidence
Medium
MeSH
Brain
MeSH
Cerebrospinal Fluid
MeSH
Serum
MeSH
Alzheimer Disease
NeuroMMSigDB
Interleukin signaling subgraph
NeuroMMSigDB
Nitric oxide subgraph

a(CHEBI:"nitric oxide") increases act(p(HGNC:CASP3)) View Subject | View Object

NO can also bring about apoptosis of hippocampal neurons via caspase- 3 activity [50] whereas astrocyte-secreted IL-1 beta can increase the production of APP and A beta from neu- rons [51–53] (Fig. 1). PubMed:27314526

Annotations
Confidence
Medium
MeSH
Hippocampus
MeSH
Alzheimer Disease
NeuroMMSigDB
Amyloidogenic subgraph
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph
NeuroMMSigDB
Nitric oxide subgraph

Sample Nodes

a(CHEBI:"amyloid-beta")

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

a(MESH:Microglia)

In-Edges: 19 | Out-Edges: 25 | Explore Neighborhood | Download JSON

bp(GO:"inflammatory response")

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

bp(GO:cognition)

In-Edges: 111 | Out-Edges: 35 | Explore Neighborhood | Download JSON

path(MESH:"Alzheimer Disease")

In-Edges: 536 | Out-Edges: 704 | Classes: 5 | 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.