Clearance of Amyloid Beta and Tau in Alzheimer’s Disease:from Mechanisms to Therapy v1.0.1

Compilation Biogrammar

Provenance

Upload: charles.hoyt@scai.fraunhofer.de at 2019-02-27 16:23:23.636949
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: 149
Number Edges: 279
Number Components: 2
Network Density: 0.0126519136586251
Average Degree: 1.87248322147651
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
Inert and seed-competent tau monomers suggest structural origins of aggregation v1.0.0	38%
Pathological missorting of endogenous MAPT/Tau in neurons caused by failure of protein degradation systems v1.0.1	33%
Estrogen receptor-α is localized to neurofibrillary tangles in Alzheimer's disease v1.0.0	33%
Identification of a novel aspartic protease (Asp 2) as beta-secretase v1.0.0	30%
Effects of peptides derived from BACE1 catalytic domain on APP processing v1.0.0	30%
Alzheimer's disease pathological lesions activate the spleen tyrosine kinase. v1.0.0	29%
Clearance systems in the brain-implications for Alzheimer disease. v1.0.1	28%
Tau Trimers Are the Minimal Propagation Unit Spontaneously Internalized to Seed Intracellular Aggregation v1.0.0	27%
Tau Antibody Targeting Pathological Species Blocks Neuronal Uptake and Interneuron Propagation of Tau in Vitro v1.0.0	27%
Pseudophosphorylation of tau at S422 enhances SDS-stable dimer formation and impairs both anterograde and retrograde fast axonal transport. v1.0.0	27%

Sample Edges

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

p(HGNC:MAPT) hasVariant p(HGNC:MAPT, frag("?")) View Subject | View Object

a(CHEBI:"(-)-epigallocatechin 3-gallate") decreases p(HGNC:MAPT, pmod(Ph)) View Subject | View Object

Epigallocatechin-3-gallate enhances the clearance of ADrelevant phosphorylated tau species via increasing mRNA expression of autophagy adaptor proteins NDP52 and p62 (Chesser et al. 2016) PubMed:29626319

a(CHEBI:"(-)-epigallocatechin 3-gallate") increases p(HGNC:CALCOCO2) View Subject | View Object

Epigallocatechin-3-gallate enhances the clearance of ADrelevant phosphorylated tau species via increasing mRNA expression of autophagy adaptor proteins NDP52 and p62 (Chesser et al. 2016) PubMed:29626319

a(CHEBI:"(-)-epigallocatechin 3-gallate") increases p(HGNC:SQSTM1) View Subject | View Object

Epigallocatechin-3-gallate enhances the clearance of ADrelevant phosphorylated tau species via increasing mRNA expression of autophagy adaptor proteins NDP52 and p62 (Chesser et al. 2016) PubMed:29626319

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

a(MESH:Monocytes)

In-Edges: 4 | Out-Edges: 7 | Explore Neighborhood | Download JSON

bp(GO:"immune response")

In-Edges: 7 | Out-Edges: 5 | Explore Neighborhood | Download JSON

bp(GO:"inflammatory response")

In-Edges: 55 | Out-Edges: 24 | 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.