In this context, differential tryptophan metabolism depending on astrocyte or microglia predominance determines the balance between tryptophan catabolites, such as neuroprotective kynurenic acid and pro-inflammatory quinolinic acid (27)
And this is like a niche, you know, pop up or something, but it's not definitely not Australian
To replicate the situation where efficacy predictions are made before treatment, we assumed the dose, treatment duration and drug type variables were unknown, and imputed these values in the model to an arbitrary constant value for all participants
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So if you take glutathione, which its job is to eat up that hydrogen peroxide, then your methylation can keep working
