Appears in Networks 1

Provenance

PubMed:16273023

In patients with Alzheimer's disease, available evidence points to a disruption in the glutamatergic neurotransmission cycle at the point of glial cell reuptake of free glutamate from the synapse. Neuropathologic studies have documented reduced levels of glutamate reuptake in the frontal and temporal cortices of patients with Alzheimer's disease,10 possibly due to oxidative modification of the glutamate transporter 1 molecule. Furthermore, diminished uptake by vesicular glutamate transporter has been reported in patients with Alzheimer's disease

Related Edges 1

Annotations 4

Cell Ontology (CL)
glial cell
Disease Ontology (DO)
Alzheimer's disease
MeSH
Frontal Lobe
MeSH
Temporal Lobe

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.