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This forward-looking perspective underscores that energy metabolism functions not merely as a support system for neuronal activity but as a pivotal regulator in brain health and disease through mechanisms such as mitochondrial ATP synthesis, calcium buffering, and oxidative stress response (Nicholls and Budd, 2000)

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This study not only elucidates the mechanisms of PARP1-mediated PXR E194 ribosylation in AILI but also identifies Sch B as the first specific inhibitor of this pathway, providing a theoretical basis for precision detoxification strategies targeting posttranslational modifications