Provenance

Upload
charles.hoyt@scai.fraunhofer.de at 2019-02-27 16:03:03.931207
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
51
Number Edges
120
Number Components
1
Network Density
0.0470588235294118
Average Degree
2.35294117647059
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
In Vivo and In Vitro Characterization of Antalarmin, a Nonpeptide Corticotropin-Releasing Hormone (CRH) Receptor Antagonist: Suppression of Pituitary ACTH Release and Peripheral Inflammation v1.0.0 20%
A role for b2* nicotinic receptors in a model of local amyloid pathology induced in dentate gyrus v1.0.0 19%
Selective activation of α7 nicotinic acetylcholine receptor by PHA-543613 improves Aβ25-35-mediated cognitive deficits in mice v1.0.0 18%
Role of the nicotinic acetylcholine receptor in Alzheimer's disease pathology and treatment v1.0.1 18%
Clearance of Amyloid Beta and Tau in Alzheimer’s Disease:from Mechanisms to Therapy v1.0.1 18%
Estrogen receptor-α is localized to neurofibrillary tangles in Alzheimer's disease v1.0.0 17%
Nuclear receptors as therapeutic targets for Alzheimer's disease. v1.0.0 16%
Nicotinic Receptor Abnormalities of Alzheimer’s Disease: Therapeutic Implications v1.0.0 16%
The Ubiquitin Proteasome System in Neurodegenerative Diseases: Sometimes the Chicken, Sometimes the Egg v1.0.0 16%
Tau Modifications v1.9.5 16%

Sample Edges

tloc(a(CHEBI:"amyloid-beta"), fromLoc(MESH:Blood), toLoc(MESH:"Cerebrospinal Fluid")) regulates deg(a(CHEBI:"amyloid-beta")) View Subject | View Object

By contrast, the parenchyma of the CNS is devoid of lymphatic vasculature2; in the brain, removal of cellular debris and toxic molecules, such as amyloid-β peptides, is mediated by a combination of transcellular transport mechanisms across the blood−brain and blood−cerebrospinal fluid (CSF) barriers7–9, phagocytosis and digestion by resident microglia and recruited monocytes and/or macrophages10,11, as well as CSF influx and ISF efflux through a paravascular (glymphatic) route12–14 PubMed:30046111

Annotations
Confidence
High
MeSH
Brain

a(CHEBI:"amyloid-beta") negativeCorrelation act(a(MESH:"Lymphatic Vessels")) View Subject | View Object

Analysis of lymphoid and myeloid cell populations in the meninges (Extended Data Fig. 9d) demonstrated a significant increase in the number of macrophages upon lymphatic ablation compared to both control groups (Extended Data Fig. 9e), which might be correlated with increased amyloid-β deposition and inflammation in the meninges PubMed:30046111

Annotations
Confidence
High
MeSH
Meninges

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

Staining for amyloid-β in the brains of nine patients with Alzheimer’s disease and eight controls without Alzheimer’s disease (Extended Data Table 1) revealed, as expected, marked parenchymal deposition of amyloid-β in the brains of patients with Alzheimer’s disease, but not in the brains of the controls without Alzheimer’s disease (Extended Data Fig. 9l, m) PubMed:30046111

Annotations
Confidence
Medium
MeSH
Brain
MeSH
Parenchymal Tissue

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

Notably, when compared to tissue from controls, all samples from patients with Alzheimer’s disease demonstrated striking vascular amyloid-β pathology in the cortical leptomeninges (Extended Data Fig. 9l, m) and amyloid-β deposition in the dura mater adjacent to the superior sagittal sinus (Fig. 3i, j) or further away from the sinus (Fig. 3k, l) PubMed:30046111

Annotations
Confidence
Medium
MeSH
Dura Mater
MeSH
Superior Sagittal Sinus

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

These findings showed that prominent meningeal amyloid-β deposition observed in patients with Alzheimer’s disease is also observed in mouse models of Alzheimer’s disease after meningeal lymphatic vessel ablation PubMed:30046111

Annotations
Confidence
Medium
MeSH
Meninges
MeSH
Alzheimer Disease

Sample Nodes

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.