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Methods: Targeted lipidomics analysis of 35 eicosanoid lipids was performed in a prospective cohort with biopsy-proven NAFLD and no CVD at baseline (n=157)

Taking these findings together, the dietary Met supplementation-mediated prevention of cognitive dysfunction potentially occurs by increasing flux via the TSP

10.1016/j.cmet.2017.11.002 384 YuB.PamphlettR

In human studies, long-term recreational ketamine use has been associated with structural brain changes, including reduced prefrontal gray matter volume and impaired white matter connectivity, which are potentially linked to chronic low-grade inflammation ( 5.2.2 Mitochondrial dysfunction Ketamine disrupts mitochondrial function by reducing the membrane potential, increasing cytochrome c release, and promoting ROS generation, which collectively induce neuronal apoptosis ( Human studies have identified metabolic abnormalities in ketamine abusers, particularly in the prefrontal cortex, which may reflect mitochondrial dysfunction ( 5.2.3 Dose and frequency dependence The neurotoxic effects of ketamine are highly dependent on its dosage and frequency of use

[DOI] [PubMed] [Google Scholar] Guzman-Chavez F