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In neurodegenerative contexts, a critical dichotomy emerges: a loss of support function contrasts with reactive, potentially inflammatory metabolic reprogramming

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The neuroprotective effects of the ketogenic diet are closely linked to its induction of metabolic remodeling and protein modification: by increasing -hydroxybutyrate levels, it specifically promotes -hydroxybutyrylation of key tricarboxylic acid (TCA) cycle enzymes (such as citrate synthase [CS] and succinate-CoA ligase subunit alpha [SUCLG1]), enhancing enzymatic activity and ATP production to improve neuronal energy metabolism

Potential E3 ligases responsible for LLPS of ubiquitinated proteins and proteasomes also need to be elucidated in the future

This upregulation of transcription factors supports the hypothesis that Georgia-03 L activates a robust transcriptional network in response to infection, coordinating several defense-related processes, including pathogen recognition, secondary metabolism, and antioxidative stress responses