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Appears in Networks 1

In-Edges 5

a(CHEBI:"NMDA receptor antagonist") association bp(GO:"GO:0035249") 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

bp(GO:"GO:0014047") increases bp(GO:"GO:0035249") View Subject | View Object

In healthy individuals, the glutamatergic neurotransmission cycle begins in the mitochondria of hippocampal neurons, where the enzyme glutaminase catalyzes the conversion of glutamine to glutamate. Next, the vesicular glutamate transporter molecule mediates the packaging of these glutamate molecules into vesicles. Glutamate-containing vesicles are then released from the neuron, resulting in elevated synaptic concentrations of free glutamate, which can transmit neural signals by interacting with glutamatergic receptors on postsynaptic neurons PubMed:16273023

path(MESH:D000544) decreases 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

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

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

Out-Edges 4

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

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

bp(GO:"GO:0035249") increases bp(GO:"GO:0051935") View Subject | View Object

Synaptic glutamate concentration is promptly restored to normal levels, however, through the rapid uptake of unbound glutamate molecules by nearby glial cells, which subsequently convert these glutamate molecules to glutamine. The resulting glutamine molecules are then recycled to the neurons, and the cycle of glutamatergic signaling begins anew PubMed:16273023

Annotations
Cell Ontology (CL)
glial cell

bp(GO:"GO:0035249") association a(CHEBI:"NMDA receptor antagonist") 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

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.