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A detailed understanding of the distinct pathophysiological mechanisms and redox imbalances underlying each neurodegenerative disorder is crucial for advancing personalized therapeutic strategies, enabling interventions tailored to the specific cellular vulnerabilities and molecular drivers of each disease

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288 Existing studies have demonstrated that L-DON and JHU-083 can extensively inhibit Gln metabolizing enzymes and activate AMPK and c-Myc to inhibit glycolysis, thereby stopping tumor metabolic activity, alleviating hypoxia, and increasing the concentration of Gln and glucose in TME

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Archived from the original on 10 July 2023