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r(HGNC:CHRNA7)

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Entity

Name
CHRNA7
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 3

Nicotinic acetylcholine receptor signalling: roles in Alzheimer's disease and amyloid neuroprotection. v1.0.0

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

Nicotinic Receptor Abnormalities of Alzheimer’s Disease: Therapeutic Implications v1.0.0

In-Edges 6

path(MESH:"Plaque, Amyloid") causesNoChange r(HGNC:CHRNA7) View Subject | View Object

Intracerebral injection of Abeta into rats resulted in a loss of alpha4 and alpha7 subunits as measured by Western blotting but an increase in alpha7 mRNA (Liu et al., 2008), again suggesting that Abeta directly reduces expression of alpha7 nAChRs through mechanisms other than reduced mRNAproduction, although caution should be exercised in interpreting quantitative data from Western blot studies. It is noteworthy that a combined patch-clamp and in situ hybridization study of dissociated human brain tissue (obtained as route-of-access tissue removed during surgery) indicated that neurons near Abeta plaques retained alpha4 and alpha7 mRNA transcripts, whereas these transcripts were absent in neurons burdened with hyperphosphorylated tau protein (Wevers et al., 1999). PubMed:19293145

Appears in Networks:

complex(a(CHEBI:"amyloid-beta"), p(HGNC:CHRNA7)) increases r(HGNC:CHRNA7) View Subject | View Object

Despite a putative beneficial role for increased CBF neuron alpha7 nAChR expression in AD (that may also be relevant to smoking behavior), evidence suggests that increased alpha7 nAChR expression contributes to cellular degeneration. Notably, alpha7 nAChR binds and/or interacts with APP and Ab peptides [123–125]. Increased NB neuronal alpha7 nAChR expression may arise as a compensatory response that is offset by aberrant Ab-alpha7 nAChR interactions, leading to cholinergic dysfunction. PubMed:18986241

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

path(MESH:D000544) increases r(HGNC:CHRNA7) View Subject | View Object

Single cell expression via microarray analysis was used to determine whether expression levels for nAChR and mAChR receptors, as well as ChAT, were differentially regulated within individual CBF neurons harvested from NCI, MCI and AD cases. ChAT mRNA expression levels did not differ across clinical conditions (Table 1). However, there was a significant upregulation of alpha7 nAChR subunit expression in AD compared with NCI and MCI. PubMed:18986241

Appears in Networks:
Annotations
MeSH
Cholinergic Neurons
MeSH
Cognitive Dysfunction

path(MESH:D000544) increases 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) 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:"Alzheimer Disease") positiveCorrelation r(HGNC:CHRNA7) View Subject | View Object

Examination of the regional expression of mRNA of the nAChR alpha4 and alpha3 subunits has shown no difference in autopsy AD brain tissue in any region analyzed (Hellstro ¨m-Lindahl et al 1999; Terzano et al 1998), whereas the level of the alpha7 mRNA was significantly higher in the hippocampus (Hellstro¨m-Lindahl et al 1999) PubMed:11230871

Appears in Networks:
Annotations
MeSH
Hippocampus

Out-Edges 4

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

r(HGNC:CHRNA7) regulates act(a(MESH:D059329)) 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
Cholinergic Neurons
MeSH
Cognitive Dysfunction

r(HGNC:CHRNA7) increases path(MESH:D009410) View Subject | View Object

Despite a putative beneficial role for increased CBF neuron alpha7 nAChR expression in AD (that may also be relevant to smoking behavior), evidence suggests that increased alpha7 nAChR expression contributes to cellular degeneration. Notably, alpha7 nAChR binds and/or interacts with APP and Ab peptides [123–125]. Increased NB neuronal alpha7 nAChR expression may arise as a compensatory response that is offset by aberrant Ab-alpha7 nAChR interactions, leading to cholinergic dysfunction. PubMed:18986241

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

r(HGNC:CHRNA7) positiveCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

Examination of the regional expression of mRNA of the nAChR alpha4 and alpha3 subunits has shown no difference in autopsy AD brain tissue in any region analyzed (Hellstro ¨m-Lindahl et al 1999; Terzano et al 1998), whereas the level of the alpha7 mRNA was significantly higher in the hippocampus (Hellstro¨m-Lindahl et al 1999) PubMed:11230871

Appears in Networks:
Annotations
MeSH
Hippocampus

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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.