Objective Glutamate-induced neuroexcitotoxicity has been implicated in the patho-genesis of several neurodegenerative diseases,including Parkinson's disease(PD)and Alzheimer's disease.Neuroexcitotoxicity occurs when excess glutamate overactivates the N-methyl-D-aspartate(NMDA)receptor(NMDAR),leading to neuronal toxicity.Visinin-like protein-1(VILIP-1)is a member of the large family of neuronal calcium sensors(NCS),which are mainly expressed in brain neurons and have multiple functions,including regulation of neuronal ion channels,neuronal growth and survival.Recent studies have revealed that VILIP-1 may serve as an emerging indica-tor of neurodegenerative diseases such as AD.This article provides a review of the mechanistic studies related to VILIP-1 in glutamate-mediated neuroexcitotoxicity.