path(HBP:Excitotoxicity)

Entity

Name

Excitotoxicity

Namespace

HBP

Namespace Version

20190222

Namespace URL

https://raw.githubusercontent.com/pharmacome/terminology/cfd2ee89d1a71126da8b5f452544b7fe43be67e7/export/hbp-names.belns

The interaction of tau with FYN may regulate the postsynaptic targeting of FYN, and thereby mediate Aβ‑induced excitotoxicity PubMed:26631930

The interaction of tau with FYN may regulate the postsynaptic targeting of FYN, and thereby mediate Aβ‑induced excitotoxicity PubMed:26631930

Genetic deficiency of tau protects against excitotoxicity caused by Aβ or other excitotoxins in mice that overexpress human amyloid precursor protein (APP), in mice that express human APP and human presenilin 1 (PS1), and in mice that express mutant Scn1a (the gene encoding the voltage-gated sodium channel subunit Nav1.1), as well as in mice lacking the voltage-gated potassium channel Kv1.1 subunit PubMed:26631930

Genetic deficiency of tau protects against excitotoxicity caused by Aβ or other excitotoxins in mice that overexpress human amyloid precursor protein (APP), in mice that express human APP and human presenilin 1 (PS1), and in mice that express mutant Scn1a (the gene encoding the voltage-gated sodium channel subunit Nav1.1), as well as in mice lacking the voltage-gated potassium channel Kv1.1 subunit PubMed:26631930

Our original cell culture results showed NAP protection against excitotoxicity over a broad concentration range, suggesting an involvement of the glutamatergic system in ADNP/NAP activity PubMed:30664622

Consequently, NF-κB is constitutively activated in the excitatory neurons of the cerebral cortex (layers 2, 4, and 5), hippocampus (granule and pyramidal neurons of CA1 and CA3), and cerebellar granule cells and this constitutive activity is indispensable for neuronal survival in response to glutamate-induced excitotoxicity PubMed:28745240