Sang Won Suh

TL;DR: Electrocyte glutamate transporters, a membrane-permeant cysteine pro-drug, normalized basal zinc levels, reduced TSQ (+) neurons and reduced ischemic neuronal death in the EAAC1(-/-) mice when delivered in a pre-treatment fashion are implicated.

TL;DR: The present study demonstrates that acamprosate attenuates TBI‐induced brain damage by depletion of vesicular glutamate and zinc levels and suggests that acamrosate may have high therapeutic potential for prevention of TBI-induced neuronal death.

TL;DR: It is demonstrated that zinc supplementation by ZC treatment increases hippocampal neurogenesis and levels of vesicular zinc, providing evidence in support of the essential role of zinc in modulating hippocampal Neurogenesis.

TL;DR: N-acetyl-l-cysteine (NAC) acts as a zinc chelator that alleviates zinc-induced neuronal death processes and restores levels of neuronal glutathione (GSH) by providing a cell-permeable source of cysteine.

TL;DR: Administration of α-GPC starting 3 weeks after seizure (late administration) improved cognitive function through reduced neuronal death and BBB disruption, and increased neurogenesis in the hippocampus, seemingly contradictory results may be attributed to both epileptogenic features and neuroprotective functions of several acetylcholine precursors.