Does aloysia gratissima prevent cellular damage induced by glutamatergic excitotoxicity?
AE attenuated QA-induced cell damage possibly involving the glutamate transport modulation through NMDAR interaction. FA shows a similar profile of neuroprotection promoted by AE. Therefore, AE treatment might be a useful strategy in preventing brain damage caused by exacerbation of glutamatergic toxicity in nervous system disorders.
The ITGB3 L33P seems to be unrelated to the development of OXLIPN, but it appears to be related to its severity.