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while the SHAM group was exposed to air during the same period of time as previously described (Al-Odat et al., 2015)

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It suppresses the TLR4/NFB pathway, restores autophagy markers (LC3-II/LC3-I ratio, beclin-1), and reduces neuroinflammatory cytokines in LPS-induced models.[7] In Alzheimers disease models, acetyl-L-carnitine completely rescued mitochondrial membrane potential and oxygen consumption rates impaired by amyloid-beta oligomers.[8] Direct comparative clinical data for systemic (non-CNS) inflammation and mitochondrial dysfunction remain limited, making definitive recommendations challenging outside neurological contexts.[9] References Comparison of the Effects of L-Carnitine and Acetyl-L-Carnitine on Carnitine Levels, Ambulatory Activity, and Oxidative Stress Biomarkers in the Brain of Old Rats

PubMed , Respiratory Research , vol

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