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Acetyl-L-carnitine is an orally active mitochondrial energy metabolism regulator and neuroprotectant that can penetrate the blood-brain barrier

This pathway can be interrupted by the introduction of VPA, which leads to a reduction of free coenzyme A, acetyl-CoA, and carnitine, and results in the decreased availability of cofactors necessary for the function of urea cycle and an increase in NH3 production.[15,16] Because VPA-induced metabolic disorders including hyperammonemia could be mediated at least in part by carnitine deficiency, it has been hypothesized that levocarnitine supplementation may prevent, correct, or attenuate these adverse effects[15,17] Several studies or isolated clinical cases have suggested the potential value of oral levocarnitine in reversing carnitine deficiency or preventing adverse effects due to VPA-induced dysfunction of beta-oxidation

doi: 10.4103/1735-5362.335174

Inflammatory response Atherosclerosis is also considered a chronic inflammatory disease because the endothelial inflammatory damage is ongoing throughout atherosclerosis progression (71)