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Activation of M1 and M4 muscarinic receptors as potential treatments for Alzheimer's disease and schizophrenia. 1.0.0

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charles.hoyt@scai.fraunhofer.de at 2019-02-27 16:13:54.020706
Authors
Rana Aldisi
Contact
charles.hoyt@scai.fraunhofer.de
Description
This file encodes the article Activation of M1 and M4 muscarinic receptors as potential treatments for Alzheimer’s disease and schizophrenia by Choi et al, 2014
License
CC BY 4.0
Copyright
Copyright © 2018 Fraunhofer Institute SCAI, All rights reserved.
Number Nodes
97
Number Edges
207
Number Components
2
Network Density
0.022229381443299
Average Degree
2.1340206185567
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
M1 muscarinic acetylcholine receptor in Alzheimer’s disease v1.0.0 43%
The alpha7 nicotinic receptor agonist 4OH-GTS-21 protects axotomized septohippocampal cholinergic neurons in wild type but not amyloid-overexpressing transgenic mice v1.0.0 31%
Nicotinic Receptor Abnormalities of Alzheimer’s Disease: Therapeutic Implications v1.0.0 29%
A role for b2* nicotinic receptors in a model of local amyloid pathology induced in dentate gyrus v1.0.0 29%
Alzheimer's Disease: Targeting the Cholinergic System v1.0.0 28%
Selective activation of α7 nicotinic acetylcholine receptor by PHA-543613 improves Aβ25-35-mediated cognitive deficits in mice v1.0.0 27%
albuquerque2009 v1.0.0 24%
Nicotinic acetylcholine receptor signalling: roles in Alzheimer's disease and amyloid neuroprotection. v1.0.0 23%
Identification of a novel aspartic protease (Asp 2) as beta-secretase v1.0.0 20%
Effects of peptides derived from BACE1 catalytic domain on APP processing v1.0.0 20%

Sample Edges

a(CHEBI:"EC 3.1.1.7 (acetylcholinesterase) inhibitor") increases bp(GO:"synaptic transmission, cholinergic") View Subject | View Object

The current primary treatments for AD symptoms are acetylcholinesterase inhibitors (AChEIs) such as donepezil, tacrine, galantamine, and rivastigmine, which potentiate cholinergic signaling.18,19 These treatments not only provide improvements in cognitive symptoms associated with AD,20,21 but also show efficacy in treating the psychiatric symptoms. PubMed:24511233

Annotations
MeSH
Alzheimer Disease

a(CHEBI:"EC 3.1.1.7 (acetylcholinesterase) inhibitor") increases bp(GO:cognition) View Subject | View Object

The current primary treatments for AD symptoms are acetylcholinesterase inhibitors (AChEIs) such as donepezil, tacrine, galantamine, and rivastigmine, which potentiate cholinergic signaling.18,19 These treatments not only provide improvements in cognitive symptoms associated with AD,20,21 but also show efficacy in treating the psychiatric symptoms. PubMed:24511233

Annotations
MeSH
Alzheimer Disease

a(CHEBI:"EC 3.1.1.7 (acetylcholinesterase) inhibitor") increases path(MESH:"Mental Processes") View Subject | View Object

The current primary treatments for AD symptoms are acetylcholinesterase inhibitors (AChEIs) such as donepezil, tacrine, galantamine, and rivastigmine, which potentiate cholinergic signaling.18,19 These treatments not only provide improvements in cognitive symptoms associated with AD,20,21 but also show efficacy in treating the psychiatric symptoms. PubMed:24511233

Annotations
MeSH
Alzheimer Disease

a(CHEBI:"EC 3.1.1.7 (acetylcholinesterase) inhibitor") association a(MESH:"Cardiovascular System") View Subject | View Object

Unfortunately, cardiovascular and gastrointestinal side effects are often observed with these treatments, effects thought to be mediated by peripherally located ACh receptors. Despite this, AChEIs remain modestly beneficial for treating AD and other forms of dementia. PubMed:24511233

a(CHEBI:"EC 3.1.1.7 (acetylcholinesterase) inhibitor") association a(MESH:"Gastrointestinal Tract") View Subject | View Object

Unfortunately, cardiovascular and gastrointestinal side effects are often observed with these treatments, effects thought to be mediated by peripherally located ACh receptors. Despite this, AChEIs remain modestly beneficial for treating AD and other forms of dementia. PubMed:24511233

Sample Nodes

a(CHEBI:"amyloid-beta")

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

bp(GO:cognition)

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

bp(GO:learning)

In-Edges: 52 | Out-Edges: 24 | Explore Neighborhood | Download JSON

bp(GO:memory)

In-Edges: 112 | Out-Edges: 33 | Explore Neighborhood | Download JSON

path(MESH:"Alzheimer Disease")

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

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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.