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  4. Alzheimer's disease

Alzheimer's disease

Name
Alzheimer's disease
Namespace Keyword
Disease
Namespace
Disease Ontology (DO)
Namespace Version
20170511
Namespace URL
https://arty.scai.fraunhofer.de/artifactory/bel/annotation/disease/disease-20170511.belanno

Sample Annotated Edges 5

a(CHEBI:"glutamate(2-)") directlyIncreases act(p(MESH:D017470)) View Subject | View Object

First, the presence of elevated neurotransmitter levels in the synapse under resting conditions can be thought of as a constant 'background signal,' leading to chronic low-level activation of glutamatergic receptors on postsynaptic neurons and possibly neuronal death. PubMed:16273023

Appears in Networks:
Annotations
MeSH
Post-Synaptic Density
Cell Ontology (CL)
glial cell
Disease Ontology (DO)
Alzheimer's disease
MeSH
Frontal Lobe
MeSH
Temporal Lobe

path(MESH:D000544) association path(MESH:D058225) View Subject | View Object

From the perspective of brain histopathology, Alzheimer's disease has three characteristic features—the appearance of beta-amyloid plaques, the presence of neurofibrillary tangles, and the loss of neuronal cells PubMed:16273023

Appears in Networks:
Annotations
Disease Ontology (DO)
Alzheimer's disease

path(MESH:D000544) decreases bp(GO:"GO:0014047") View Subject | View Object

Second, because of this background signal, as well as the fact that neurons are left with smaller amounts of neurotransmitter to release into the synapse during neuronal firing, the 'peak signal'—the difference between synaptic glutamate concentration during neuronal activity and synaptic glutamate concentration under resting conditions—is attenuated, leading to suboptimal neurotransmission as exemplified by a lack of long-term potentiation (LTP) PubMed:16273023

Appears in Networks:
Annotations
Cell Ontology (CL)
glial cell
Disease Ontology (DO)
Alzheimer's disease
MeSH
Frontal Lobe
MeSH
Temporal Lobe

path(MESH:D000544) decreases bp(GO:"GO:0035249") View Subject | View Object

Among the systems affected in patients with Alzheimer's disease are the cholinergic and glutamatergic neurotransmission systems. These two systems play key roles in cognition and, as a result, contemporary pharmacologic agents used in the treatment of Alzheimer's disease are designed to restore their functioning PubMed:16273023

Appears in Networks:
Annotations
Disease Ontology (DO)
Alzheimer's disease

bp(GO:"GO:0014047") increases bp(MESH:D017774) View Subject | View Object

Second, because of this background signal, as well as the fact that neurons are left with smaller amounts of neurotransmitter to release into the synapse during neuronal firing, the 'peak signal'—the difference between synaptic glutamate concentration during neuronal activity and synaptic glutamate concentration under resting conditions—is attenuated, leading to suboptimal neurotransmission as exemplified by a lack of long-term potentiation (LTP) PubMed:16273023

Appears in Networks:
Annotations
Cell Ontology (CL)
glial cell
Disease Ontology (DO)
Alzheimer's disease
MeSH
Frontal Lobe
MeSH
Temporal Lobe

Showing 5 of 226 edges

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.