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Article

Targeting glutamatergic and cellular prion protein mechanisms of amyloid β-mediated persistent synaptic plasticity disruption: Longitudinal studies.

Neuropharmacology - 15 Jul 2017

Zhang Dainan, Qi Yingjie, Klyubin Igor, Ondrejcak Tomas, Sarell Claire J, Cuello A Claudio, Collinge John, Rowan Michael J

Abstract excerpt

Alzheimer's disease amyloid-β (Aβ) oligomers are synaptotoxic, inappropriately increasing extracellular glutamate concentration and glutamate receptor activation to thereby rapidly disrupt synaptic plasticity. Thus, acutely promoting brain glutamate homeostasis with a blood-based scavenging system, glutamate-oxaloacetate transaminase (GOT), and blocking metabotropic glutamate 5 (mGlu5) receptor or its co-receptor...

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Source

Identifiers

PMID: 28390893
DOI: 10.1016/j.neuropharm.2017.03.036

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

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