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Thus, our findings are likely the result of the potent antioxidant capacity of GSH facilitating the engagement of accumbal circuitry to produce motivated behavior, as well as GSH-independent mechanisms involving more complex and long-term modifications, including a reshaping of synaptic glutamatergic activity

In a demyelination mouse model with neuroinflammation, KD treatment inhibits the activation of pro-inflammatory glial cells and decreases the production of pro-inflammatory cytokines, including IL-1 and TNF-, in addition to significantly reducing histone deacetylase 3 and NLRP3 (151)

Patients should maintain adequate hydration and seek medical attention if they notice concerning changes