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In this context, ketones offer a vital advantage: they bypass Complex I, providing threatened neurons with an alternative fuel source while simultaneously enhancing overall mitochondrial function and increasing ATP production [59]
Despite distinct primary targets, both converge on inhibiting acetyl-CoA carboxylase (ACC1), elevating acetyl-CoA levels, preserving mitochondrial homeostasis, and ultimately blocking ferroptotic cell death
Inflammatory and Cholesterol Risk in the FOURIER Trial
