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Cholinergic Neurons

Name
Cholinergic Neurons
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

path(MESH:D060825) association bp(HBP:Neurodegeneration) View Subject | View Object

Delaying or preventing cholinergic neurodegeneration or minimizing its consequences is the mechanism of action for most currently available US FDA-approved drugs for the treatment of cognitive dysfunction observed in AD [17] PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cholinergic Neurons

a(HBP:"Tau C3") biomarkerFor path(MESH:D059329) View Subject | View Object

CBF neurons displaying the tau C3 epitope, a marker for early stage NFT formation, were often hyperinnervated by GAL-containing fibers, whereas CBF neurons displaying the tau epitope MN423, an end-stage NFT marker, were not associated with GAL. Single cell gene expression studies have demonstrated that the levels of mRNAs encoding select subclasses of PP1 subunits (e.g., PP1alpha and PP1gamma) are stable in GAL hyperinnervated but downregulated in non-hyperinnervated CBF neurons in AD [149] PubMed:18986241

Appears in Networks:
Annotations
Disease Ontology (DO)
Alzheimer's disease
MeSH
Cholinergic Neurons
MeSH
Cognitive Dysfunction

path(MESH:D000544) increases path(MESH:D016874) View Subject | View Object

Cortical and CBF neurons display NFT formation in the MCI brain [9,139,140], suggesting a concomitant alteration in tau gene expression during the early stage of AD. The adult human brain contains six tau isoforms ranging from 48 to 67 kDa, which are expressed through alternative splicing of a single tau gene on chromosome 17 [141,142]. Three of these tau isoforms contain three tandem repeats in the carboxy-terminus end of the molecule (3Rtau), while three isoforms display four tandem repeats (4Rtau) in this region. Expression levels of the six tau transcripts within CBF neurons do not differ significantly during the progression of AD [6] PubMed:18986241

Appears in Networks:
Annotations
Disease Ontology (DO)
Alzheimer's disease
MeSH
Cerebral Cortex
MeSH
Cholinergic Neurons
MeSH
Cognitive Dysfunction

path(MESH:D000544) causesNoChange r(HGNC:MAPT) View Subject | View Object

Cortical and CBF neurons display NFT formation in the MCI brain [9,139,140], suggesting a concomitant alteration in tau gene expression during the early stage of AD. The adult human brain contains six tau isoforms ranging from 48 to 67 kDa, which are expressed through alternative splicing of a single tau gene on chromosome 17 [141,142]. Three of these tau isoforms contain three tandem repeats in the carboxy-terminus end of the molecule (3Rtau), while three isoforms display four tandem repeats (4Rtau) in this region. Expression levels of the six tau transcripts within CBF neurons do not differ significantly during the progression of AD [6] PubMed:18986241

Appears in Networks:
Annotations
Disease Ontology (DO)
Alzheimer's disease
MeSH
Cerebral Cortex
MeSH
Cholinergic Neurons
MeSH
Cognitive Dysfunction

g(HGNC:NTRK3) association path(MESH:D003071) View Subject | View Object

These studies have demonstrated a significant downregulation of trkA, trkB and trkC gene expression during the development of AD [7]. An intermediate reduction was observed in MCI, with the greatest decrement in mild AD compared to aged controls. Moreover, two separate expressed sequence tag (EST) cDNAs for each trk gene (e.g., ESTs targeted to the extracellular domain [ECD] and tyrosine kinase [TK]) domains were downregulated. By contrast, there was a lack of regulation of p75NTR expression [7] in CBF neurons. A ‘step down’ dysregulation of trk expression may, in part, underlie CBF neuron demise associated with the clinical presentation of AD. Supporting this concept is the finding that trk downregulation is associated with measures of cognitive decline [7,14] PubMed:18986241

Appears in Networks:
Annotations
MeSH
Basal Forebrain
MeSH
Cholinergic Neurons
MeSH
Cognitive Dysfunction

Showing 5 of 33 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.