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Amyloid β oligomers (AβOs) in Alzheimer’s disease 1.0.0

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charles.hoyt@scai.fraunhofer.de at 2019-02-27 16:11:58.240620
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
57
Number Edges
97
Number Components
1
Network Density
0.0303884711779449
Average Degree
1.70175438596491
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 33%
A role for b2* nicotinic receptors in a model of local amyloid pathology induced in dentate gyrus v1.0.0 29%
Promoting the clearance of neurotoxic proteins in neurodegenerative disorders of ageing v1.0.0 26%
The Ubiquitin–Proteasome System and the Autophagic–Lysosomal System in Alzheimer Disease v1.0.0 26%
M1 muscarinic acetylcholine receptor in Alzheimer’s disease v1.0.0 23%
Nicotinic acetylcholine receptor signalling: roles in Alzheimer's disease and amyloid neuroprotection. v1.0.0 23%
Role of the nicotinic acetylcholine receptor in Alzheimer's disease pathology and treatment v1.0.1 21%
Amyloid-Binding Alcohol Dehydrogenase (ABAD) Inhibitors for the Treatment of Alzheimer’s Disease v1.0.0 21%
Identification of a novel aspartic protease (Asp 2) as beta-secretase v1.0.0 20%
Inflammasome Involvement in Alzheimer’s Disease v1.0.0 20%

Sample Edges

a(CHEBI:"amyloid fibril") causesNoChange bp(GO:memory) View Subject | View Object

It was also demonstrated that fibril-free AβO solutions are essential for memory loss (Brito-Moreira et al. 2017), while the fibrillar Aβ in amyloid deposits is not the active factor affecting the cognition (Martins et al. 2008). PubMed:29196815

Annotations
Confidence
High

a(CHEBI:"amyloid fibril") positiveCorrelation a(HBP:HBP00074) View Subject | View Object

In addition, the load of AβO deposits significantly correlated with fibrillar Aβ plaque deposition as well as with neuronal loss and numbers of astrocytes, although not with memory deficits. PubMed:29196815

Annotations
MeSH
Extracellular Space
Cell Ontology (CL)
neuron
Confidence
High

a(CHEBI:"amyloid-beta polypeptide 42") negativeCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

Despite enhanced Aβ42 accumulation in AD brain (Lewczuk et al. 2003), concentrations of monomeric Aβ42 in the CSF of AD patients are decreased PubMed:29196815

Annotations
MeSH
Extracellular Space
Cell Ontology (CL)
neuron
Confidence
High
MeSH
Hippocampus

a(CHEBI:"amyloid-beta") positiveCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

The histopathological changes in the brain include the presence of extracellular amyloid plaques consisted of various peptide variants of amyloid β (Aβ) and accumulation of intracellular neurofibrillary tangles (NFTs) composed mainly of phosphorylated Tau proteins (pTau), localized predominantly in neurons (reviewed by Serrano-Pozo et al. 2011). PubMed:29196815

Annotations
Confidence
Medium

a(CHEBI:"amyloid-beta") positiveCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

Amyloid hypothesis is supported by the fact that progressive Aβ deposition is observed in early, preclinical stages of AD and, finally, in all AD patients. PubMed:29196815

Annotations
Confidence
High

Sample Nodes

a(CHEBI:"amyloid-beta")

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

a(HBP:HBP00018)

In-Edges: 35 | Out-Edges: 8 | Explore Neighborhood | Download JSON

bp(GO:"neuronal signal transduction")

In-Edges: 3 | Out-Edges: 2 | Explore Neighborhood | Download JSON

bp(GO:aging)

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

bp(GO:cognition)

In-Edges: 111 | Out-Edges: 35 | 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.