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The aims of this review are (1) to provide an overview of the clinical and biological overlap between neuropsychiatric long COVID and other fatigue-associated neuropsychiatric disorders, (2) to examine the shared molecular mechanisms of fatigue and depressive symptoms involving acetylcarnitine metabolism, and finally (3) to review the current evidence on acetylcarnitine supplementation studies as a treatment for fatigue-associated syndromes and pharmacological aspects of acetylcarnitine supplementation to provide a conceptual foundation for acetylcarnitine supplementation in neuropsychiatric long COVID syndrome

In the nervous system, Ca 2+ release into the cytosol through the mPTP activates neurotransmitter release by triggering vesicle exocytosis [186, 187]

Unlike DON, BPTES can also inhibit phosphorylated GLS (Katt et al., 2012)

PPAR is also involved in carnitine transport and uptake processes, and treatment with its activator increases the transcript levels of OCTN2 and OCTN3 [195, 196]