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By inhibiting the folate cycle and de novo purine synthesis, MOTS-c triggers an AMPK-driven shift that encourages the body to burn fuel rather than store it

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GSH depletion and concomitant increase in O&NS and mitochondrial dysfunctions play a role in the pathophysiology of diverse neuroimmune disorders, including depression, myalgic encephalomyelitis/chronic fatigue syndrome and Parkinsons disease, suggesting that depleted GSH is an integral part of these diseases