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5C, D and Supplementary Figs

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Given the prominent role of inflammation, oxidative stress, and mitochondrial dysfunction in MS pathophysiology, metabolic interventions aimed at enhancing mitochondrial function and providing an alternative energy source, such as the KD, have been explored as potential adjunctive strategies to slow disease progression and improve clinical outcomes (Table 5)

Mitochondrial redox control For mitochondrial redox control, the rationale is that reverse electron transport (RET) at complex I, sustained elevation of m, Ca overload and high-flux activity at the I_Q/III_Qo sites generate matrix and intermembrane-space ROS bursts that flip physiological signalling into damage during stress states such as ischemiareperfusion (Gibbs et al