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path(MESH:D003071)

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Entity

Name
D003071
Namespace
mesh
Namespace Version
20180828
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/1b20f0637c395f8aa89c2e2e342d7b704062c242/external/mesh.belns

Appears in Networks 2

Interplay of neurotransmitters in Alzheimer's disease v1.0.0

Cholinergic system during the progression of Alzheimer’s disease: therapeutic implications v1.0.0

In-Edges 11

bp(GO:"GO:0007271") association path(MESH:D003071) 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:0007271") association path(MESH:D003071) View Subject | View Object

Glutamatergic and cholinergic abnormalities are strongly correlated with cognitive deterioration in Alzheimer's disease, and both types of abnormalities have been hypothesized to have a causative role in this deterioration. The two major classes of agents used to treat cognitive symptoms of Alzheimer's disease are ChEIs and NMDA receptor antagonists. PubMed:16273023

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

bp(GO:"GO:0035249") association path(MESH:D003071) 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:0035249") association path(MESH:D003071) View Subject | View Object

Glutamatergic and cholinergic abnormalities are strongly correlated with cognitive deterioration in Alzheimer's disease, and both types of abnormalities have been hypothesized to have a causative role in this deterioration. The two major classes of agents used to treat cognitive symptoms of Alzheimer's disease are ChEIs and NMDA receptor antagonists. PubMed:16273023

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

g(HGNC:NTRK1) 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

g(HGNC:NTRK2) 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

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

p(HGNC:BCHE) association path(MESH:D003071) View Subject | View Object

Butyrylcholinesterase (BChE) is a serine hydrolase similar to AChE that is widely distributed throughout the CNS and also catalyzes the hydrolysis of ACh. BChE is localized to neurons and glia, and is associated with NFTs and senile plaques (SPs) in AD brain [32]. Interestingly, population-based genetic studies of AD have identified a point mutation that changes Ala539 to threonine in the K variant of BChE, which effectively reduces serum BChE concentrations, and may be associated with cognitive decline [33]. BChE activity also increases in AD brain whereas AChE activity remains unchanged or declines [34,35]. PubMed:18986241

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

act(p(HGNC:GAL)) association path(MESH:D003071) View Subject | View Object

For example, the neuropeptide GAL, which functions via the interaction with three G protein-coupled receptors termed GALR1, GALR2 and GALR3, has multiple biological actions, including effects on cognition and neuroplasticity [15,146,147]. In the late [148–150] but not early [151] stage of AD, fibers within the basal forebrain containing the neuropeptide GAL thicken and hyperinnervate surviving CBF neurons. Although animal and cell-culture studies have shown that GAL plays a crucial role in the regulation of CBF neuron activity [152] and rescues cholinergic cells from amyloid toxicity [153], the molecular consequences of this unique plasticity response upon CBF neurons in AD remain unclear. Gene expression studies of cholinergic transcripts have shown that GAL hyperinnervated, but not nonhyperinnervated, CBF neurons display an upregulation of ChAT expression in AD compared to controls [126] PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cognitive Dysfunction

path(MESH:D000544) association path(MESH:D003071) View Subject | View Object

Alzheimer’s disease (AD) is a progressive and fatal neurodegenerative disorder manifested by cognitive and memory decline and progressive impairment of activities of daily living, as well as a variety of neuropsychiatric symptoms and behavioral dysfunctions. PubMed:18986241

Appears in Networks:

r(HGNC:CHRNA7) negativeCorrelation path(MESH:D003071) View Subject | View Object

This increase in alpha7 nAChR expression levels within CBF neurons was inversely associated with cognitive performance. Increased alpha7 nAChR expression in CBF neurons may signal a compensatory response to maintain basocortical cholinergic activity during the onset of AD. Upregulation of the alpha7 nAChR within individual CBF neurons is also consistent with reports of increased alpha7 nAChR mRNA and protein expression levels in hippocampal neurons, astrocytes and peripheral blood leukocytes in AD [120–122]. The observed increase in alpha7 nAChR in early AD may regulate basocortical cholinergic tone through pre- and/or postsynaptic mechanisms within cholinergic NB neurons prior to their frank degeneration in the later stages of AD. PubMed:18986241

Appears in Networks:
Annotations
Disease Ontology (DO)
Alzheimer's disease
MeSH
Astrocytes
MeSH
Hippocampus
MeSH
Leukocytes
MeSH
Cognitive Dysfunction

Out-Edges 11

path(MESH:D003071) association bp(GO:"GO:0007271") View Subject | View Object

Glutamatergic and cholinergic abnormalities are strongly correlated with cognitive deterioration in Alzheimer's disease, and both types of abnormalities have been hypothesized to have a causative role in this deterioration. The two major classes of agents used to treat cognitive symptoms of Alzheimer's disease are ChEIs and NMDA receptor antagonists. PubMed:16273023

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

path(MESH:D003071) association 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

path(MESH:D003071) association bp(GO:"GO:0035249") View Subject | View Object

Glutamatergic and cholinergic abnormalities are strongly correlated with cognitive deterioration in Alzheimer's disease, and both types of abnormalities have been hypothesized to have a causative role in this deterioration. The two major classes of agents used to treat cognitive symptoms of Alzheimer's disease are ChEIs and NMDA receptor antagonists. PubMed:16273023

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

path(MESH:D003071) association bp(GO:"GO:0007271") 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

path(MESH:D003071) association path(MESH:D000544) View Subject | View Object

Alzheimer’s disease (AD) is a progressive and fatal neurodegenerative disorder manifested by cognitive and memory decline and progressive impairment of activities of daily living, as well as a variety of neuropsychiatric symptoms and behavioral dysfunctions. PubMed:18986241

Appears in Networks:

path(MESH:D003071) association p(HGNC:BCHE) View Subject | View Object

Butyrylcholinesterase (BChE) is a serine hydrolase similar to AChE that is widely distributed throughout the CNS and also catalyzes the hydrolysis of ACh. BChE is localized to neurons and glia, and is associated with NFTs and senile plaques (SPs) in AD brain [32]. Interestingly, population-based genetic studies of AD have identified a point mutation that changes Ala539 to threonine in the K variant of BChE, which effectively reduces serum BChE concentrations, and may be associated with cognitive decline [33]. BChE activity also increases in AD brain whereas AChE activity remains unchanged or declines [34,35]. PubMed:18986241

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

path(MESH:D003071) association g(HGNC:NTRK1) 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

path(MESH:D003071) association g(HGNC:NTRK2) 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

path(MESH:D003071) association g(HGNC:NTRK3) 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

path(MESH:D003071) negativeCorrelation r(HGNC:CHRNA7) View Subject | View Object

This increase in alpha7 nAChR expression levels within CBF neurons was inversely associated with cognitive performance. Increased alpha7 nAChR expression in CBF neurons may signal a compensatory response to maintain basocortical cholinergic activity during the onset of AD. Upregulation of the alpha7 nAChR within individual CBF neurons is also consistent with reports of increased alpha7 nAChR mRNA and protein expression levels in hippocampal neurons, astrocytes and peripheral blood leukocytes in AD [120–122]. The observed increase in alpha7 nAChR in early AD may regulate basocortical cholinergic tone through pre- and/or postsynaptic mechanisms within cholinergic NB neurons prior to their frank degeneration in the later stages of AD. PubMed:18986241

Appears in Networks:
Annotations
Disease Ontology (DO)
Alzheimer's disease
MeSH
Astrocytes
MeSH
Hippocampus
MeSH
Leukocytes
MeSH
Cognitive Dysfunction

path(MESH:D003071) association act(p(HGNC:GAL)) View Subject | View Object

For example, the neuropeptide GAL, which functions via the interaction with three G protein-coupled receptors termed GALR1, GALR2 and GALR3, has multiple biological actions, including effects on cognition and neuroplasticity [15,146,147]. In the late [148–150] but not early [151] stage of AD, fibers within the basal forebrain containing the neuropeptide GAL thicken and hyperinnervate surviving CBF neurons. Although animal and cell-culture studies have shown that GAL plays a crucial role in the regulation of CBF neuron activity [152] and rescues cholinergic cells from amyloid toxicity [153], the molecular consequences of this unique plasticity response upon CBF neurons in AD remain unclear. Gene expression studies of cholinergic transcripts have shown that GAL hyperinnervated, but not nonhyperinnervated, CBF neurons display an upregulation of ChAT expression in AD compared to controls [126] PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cognitive Dysfunction

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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.