1. Catalog
  2. Namespaces
  3. MeSH
  4. Frontal Lobe

Frontal Lobe

Name
Frontal Lobe
Namespace Keyword
MeSHAnatomy
Namespace
MeSH
Namespace Version
20170511
Namespace URL
https://arty.scai.fraunhofer.de/artifactory/bel/annotation/mesh-anatomy/mesh-anatomy-20170511.belanno

Sample Annotated Edges 5

a(MESH:"Cholinergic Neurons") increases act(p(HGNC:CHAT)) View Subject | View Object

Loss of cholinergic neurons has often been demonstrated as lowered ChAT activity in brains of patients with AD. Early post mortem studies indicated a loss of ChAT activity restricted to the neocortex (Slotkin et al., 1990) and this has been confirmed in more recent studies on frontal lobe and temporal cortex (Lai et al., 2006). It is noteworthy that an increase in ChAT activity in the surviving neurons was interpreted as a possible compensatory mechanism (Slotkin et al., 1990). PubMed:19293145

Appears in Networks:
Annotations
MeSH
Frontal Lobe
MeSH
Neocortex
MeSH
Temporal Lobe

path(MESH:"Alzheimer Disease") decreases a(MESH:"Cholinergic Neurons") View Subject | View Object

Loss of cholinergic neurons has often been demonstrated as lowered ChAT activity in brains of patients with AD. Early post mortem studies indicated a loss of ChAT activity restricted to the neocortex (Slotkin et al., 1990) and this has been confirmed in more recent studies on frontal lobe and temporal cortex (Lai et al., 2006). It is noteworthy that an increase in ChAT activity in the surviving neurons was interpreted as a possible compensatory mechanism (Slotkin et al., 1990). PubMed:19293145

Appears in Networks:
Annotations
MeSH
Frontal Lobe
MeSH
Neocortex
MeSH
Temporal Lobe

path(MESH:"Alzheimer Disease") decreases act(complex(p(HGNC:CHRNA4), p(HGNC:CHRNB2))) View Subject | View Object

Binding studies using subtypeselective labeled ligands suggest that alpha4beta2 receptors are lost in brains from patients with AD (Warpman and Nordberg, 1995; Martin-Ruiz et al., 1999). Regions showing reduced binding levels include the frontal lobe and the temporal cortex (Lai et al., 2006). PubMed:19293145

Appears in Networks:
Annotations
MeSH
Brain
MeSH
Frontal Lobe
MeSH
Temporal Lobe

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) 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

Showing 5 of 49 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.