What would be pharmacologically relevant explanatory factors? Could it be due to Glutamate NMDA excitotoxicity via co-agonism? Or toxic Glyr inhibition overload

What would be pharmacologically relevant explanatory factors? Could it be due to Glutamate NMDA excitotoxicity via co-agonism? Or toxic Glyr inhibition overload? The researchers should answer wether said hypothethical neurotoxicity would also apply to the co-agonist Glycine. Although I seriously doubt serine overload beind a causative factor, the excitotoxicity should be cancelled by Glyr inhibition and by default should be negligible? > The biosynthesis of serine starts with the oxidation of 3-phosphoglycerate (an intermediate from glycolysis) to 3-phosphohydroxypyruvate and NADH by phosphoglycerate dehydrogenase (EC 1.1.1.95). Could an oxitative stress overload potentiate this reaction?