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a(MESH:D002800)

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Entity

Name
D002800
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 7

bp(GO:"GO:0007271") association a(MESH:D002800) View Subject | View Object

ChEIs are believed to target cholinergic abnormalities in Alzheimer's disease, although there is evidence indicating that their therapeutic effect may be via the glutamatergic system. NMDA receptor antagonists, in contrast, are believed to target the glutamatergic system directly PubMed:16273023

Appears in Networks:

bp(GO:"GO:0050435") association a(MESH:D002800) View Subject | View Object

Recent studies report that anticholinesterase drugs reduce circulating Ab deposition in several dementia types, including AD [159]. Evidence from clinical trials [160], noninvasive functional imaging [161] and basic science research suggest that cholinesterase inhibitors might alter APP processing and therefore provide some degree of neuroprotection [162,163] PubMed:18986241

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

path(MESH:D000855) association a(MESH:D002800) View Subject | View Object

Since the cholinergic deficit is not an early defect in the progression of AD [18–20], the use of these drugs in the prodromal stages of AD should be continued. However, the limited effect of cholinesterase inhibitors for the treatment of cognitive decline in AD coupled with unwanted side effects such as diarrhea, nausea, insomnia, fatigue and loss of appetite indicates the need to move beyond this conventional drug treatment with somewhat circumscribed efficacy. PubMed:18986241

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

path(MESH:D003967) association a(MESH:D002800) View Subject | View Object

Since the cholinergic deficit is not an early defect in the progression of AD [18–20], the use of these drugs in the prodromal stages of AD should be continued. However, the limited effect of cholinesterase inhibitors for the treatment of cognitive decline in AD coupled with unwanted side effects such as diarrhea, nausea, insomnia, fatigue and loss of appetite indicates the need to move beyond this conventional drug treatment with somewhat circumscribed efficacy. PubMed:18986241

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

path(MESH:D005221) association a(MESH:D002800) View Subject | View Object

Since the cholinergic deficit is not an early defect in the progression of AD [18–20], the use of these drugs in the prodromal stages of AD should be continued. However, the limited effect of cholinesterase inhibitors for the treatment of cognitive decline in AD coupled with unwanted side effects such as diarrhea, nausea, insomnia, fatigue and loss of appetite indicates the need to move beyond this conventional drug treatment with somewhat circumscribed efficacy. PubMed:18986241

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

path(MESH:D007319) association a(MESH:D002800) View Subject | View Object

Since the cholinergic deficit is not an early defect in the progression of AD [18–20], the use of these drugs in the prodromal stages of AD should be continued. However, the limited effect of cholinesterase inhibitors for the treatment of cognitive decline in AD coupled with unwanted side effects such as diarrhea, nausea, insomnia, fatigue and loss of appetite indicates the need to move beyond this conventional drug treatment with somewhat circumscribed efficacy. PubMed:18986241

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

path(MESH:D009325) association a(MESH:D002800) View Subject | View Object

Since the cholinergic deficit is not an early defect in the progression of AD [18–20], the use of these drugs in the prodromal stages of AD should be continued. However, the limited effect of cholinesterase inhibitors for the treatment of cognitive decline in AD coupled with unwanted side effects such as diarrhea, nausea, insomnia, fatigue and loss of appetite indicates the need to move beyond this conventional drug treatment with somewhat circumscribed efficacy. PubMed:18986241

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

Out-Edges 13

a(MESH:D002800) increases bp(GO:"GO:0014047") View Subject | View Object

Pyramidal neurons, which account for ~70% of all neurons in the neocortex, use glutamate as their primary neurotransmitter. Nonetheless, in addition to possessing glutamatergic receptors on their surface, these neurons often also possess cholinergic receptors, which are capable of receiving cholinergic inputs into the neocortex from the basal forebrain. The presence of these cholinergic receptors has been putatively linked to an important finding regarding the interaction between the cholinergic and glutamatergic neurotransmission systems. In particular, rodent studies have revealed that cholinesterase inhibitors (ChEIs) promote the release of glutamate from pyramidal neurons,16 with the proposed explanation being that ChEI administration leads to increased cortical ACh concentrations and, consequently, increased binding of ACh by cholinergic receptors on pyramidal neurons, thereby stimulating neuronal firing (ie, glutamate release). PubMed:16273023

Appears in Networks:
Annotations
Cell Ontology (CL)
pyramidal neuron
MeSH
Neocortex

a(MESH:D002800) increases bp(GO:"GO:0014047") View Subject | View Object

With regard to the glutamatergic system, studies suggest that ChEIs may stimulate the release of glutamate from pyramidal neurons during normal neuronal activity, while NMDA receptor antagonists are believed to block the abnormal neuronal activity that results from the presence of excess glutamate in the synapse under resting conditions. Thus, ChEIs and NMDA receptor antagonists appear to have complementary effects, as the former enhance the signals received by postsynaptic neurons during normal neurotransmission, and the latter diminish the background 'noise' that is constantly being detected by those same receptors. PubMed:16273023

Appears in Networks:
Annotations
Cell Ontology (CL)
pyramidal neuron

a(MESH:D002800) increases a(CHEBI:acetylcholine) View Subject | View Object

Pyramidal neurons, which account for ~70% of all neurons in the neocortex, use glutamate as their primary neurotransmitter. Nonetheless, in addition to possessing glutamatergic receptors on their surface, these neurons often also possess cholinergic receptors, which are capable of receiving cholinergic inputs into the neocortex from the basal forebrain. The presence of these cholinergic receptors has been putatively linked to an important finding regarding the interaction between the cholinergic and glutamatergic neurotransmission systems. In particular, rodent studies have revealed that cholinesterase inhibitors (ChEIs) promote the release of glutamate from pyramidal neurons,16 with the proposed explanation being that ChEI administration leads to increased cortical ACh concentrations and, consequently, increased binding of ACh by cholinergic receptors on pyramidal neurons, thereby stimulating neuronal firing (ie, glutamate release). PubMed:16273023

Appears in Networks:
Annotations
Cell Ontology (CL)
pyramidal neuron
MeSH
Neocortex

a(MESH:D002800) association bp(GO:"GO:0007271") View Subject | View Object

ChEIs are believed to target cholinergic abnormalities in Alzheimer's disease, although there is evidence indicating that their therapeutic effect may be via the glutamatergic system. NMDA receptor antagonists, in contrast, are believed to target the glutamatergic system directly PubMed:16273023

Appears in Networks:

a(MESH:D002800) decreases path(MESH:D000544) View Subject | View Object

Notably, reports that physostigmine and oral anticholinesterases have beneficial effects for patients with AD suggest that the CBF system is somewhat preserved during the progression of dementia, despite well-documented loss of cholinergic biosynthetic machinery (including ChAT and AChE enzyme deficits) in patients with this disease. Interestingly, recent studies have shown that ChAT activity, which results in acetylcholine (ACh) synthesis, is preserved in the neocortex of people with MCI [18,19]. PubMed:18986241

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

a(MESH:D002800) decreases a(CHEBI:"amyloid-beta") View Subject | View Object

Recent studies report that anticholinesterase drugs reduce circulating Ab deposition in several dementia types, including AD [159]. Evidence from clinical trials [160], noninvasive functional imaging [161] and basic science research suggest that cholinesterase inhibitors might alter APP processing and therefore provide some degree of neuroprotection [162,163] PubMed:18986241

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

a(MESH:D002800) increases bp(MESH:D000066829) View Subject | View Object

Recent studies report that anticholinesterase drugs reduce circulating Ab deposition in several dementia types, including AD [159]. Evidence from clinical trials [160], noninvasive functional imaging [161] and basic science research suggest that cholinesterase inhibitors might alter APP processing and therefore provide some degree of neuroprotection [162,163] PubMed:18986241

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

a(MESH:D002800) association bp(GO:"GO:0050435") View Subject | View Object

Recent studies report that anticholinesterase drugs reduce circulating Ab deposition in several dementia types, including AD [159]. Evidence from clinical trials [160], noninvasive functional imaging [161] and basic science research suggest that cholinesterase inhibitors might alter APP processing and therefore provide some degree of neuroprotection [162,163] PubMed:18986241

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

a(MESH:D002800) association path(MESH:D007319) View Subject | View Object

Since the cholinergic deficit is not an early defect in the progression of AD [18–20], the use of these drugs in the prodromal stages of AD should be continued. However, the limited effect of cholinesterase inhibitors for the treatment of cognitive decline in AD coupled with unwanted side effects such as diarrhea, nausea, insomnia, fatigue and loss of appetite indicates the need to move beyond this conventional drug treatment with somewhat circumscribed efficacy. PubMed:18986241

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

a(MESH:D002800) association path(MESH:D003967) View Subject | View Object

Since the cholinergic deficit is not an early defect in the progression of AD [18–20], the use of these drugs in the prodromal stages of AD should be continued. However, the limited effect of cholinesterase inhibitors for the treatment of cognitive decline in AD coupled with unwanted side effects such as diarrhea, nausea, insomnia, fatigue and loss of appetite indicates the need to move beyond this conventional drug treatment with somewhat circumscribed efficacy. PubMed:18986241

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

a(MESH:D002800) association path(MESH:D009325) View Subject | View Object

Since the cholinergic deficit is not an early defect in the progression of AD [18–20], the use of these drugs in the prodromal stages of AD should be continued. However, the limited effect of cholinesterase inhibitors for the treatment of cognitive decline in AD coupled with unwanted side effects such as diarrhea, nausea, insomnia, fatigue and loss of appetite indicates the need to move beyond this conventional drug treatment with somewhat circumscribed efficacy. PubMed:18986241

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

a(MESH:D002800) association path(MESH:D005221) View Subject | View Object

Since the cholinergic deficit is not an early defect in the progression of AD [18–20], the use of these drugs in the prodromal stages of AD should be continued. However, the limited effect of cholinesterase inhibitors for the treatment of cognitive decline in AD coupled with unwanted side effects such as diarrhea, nausea, insomnia, fatigue and loss of appetite indicates the need to move beyond this conventional drug treatment with somewhat circumscribed efficacy. PubMed:18986241

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

a(MESH:D002800) association path(MESH:D000855) View Subject | View Object

Since the cholinergic deficit is not an early defect in the progression of AD [18–20], the use of these drugs in the prodromal stages of AD should be continued. However, the limited effect of cholinesterase inhibitors for the treatment of cognitive decline in AD coupled with unwanted side effects such as diarrhea, nausea, insomnia, fatigue and loss of appetite indicates the need to move beyond this conventional drug treatment with somewhat circumscribed efficacy. PubMed:18986241

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