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Rg1 can effectively alleviate PD-associated motor and cognitive dysfunctions through various mechanisms, including the inhibition of neuroinflammation, reduction of oxidative stress, promotion of neuronal survival, and enhancement of synaptic plasticity

Tumor heterogeneity further complicates this landscape, as the extent of GSH dependency varies across tumor types, metabolic states, and microenvironments, with poorly defined consequences for therapeutic response

Current Medical Chemistry

Bases, on the other hand, can be more difficult to detect
ChREBP mediates carbohydrate, but not fat-induced DNL as high fat diets do not activate ChREBP and may even decrease ChREBP activity [43, 47]
