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The therapeutic use of PE in GBS is theoretically justified by the need to remove neuro-toxic inflammatory agents that cause the condition following preceding infection, and mechanisms of molecular mimicry, established in axonal forms, as described above

According to Cant et al., Cell Metabolism , increased NAD stimulates PGC-1 activity, driving mitochondrial biogenesis and substrate flexibility

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These drawbacks highlight the necessity for more consistent reporting of results and improved coordination between preclinical and clinical evidence streams

Damage can occur if the injection site is not mapped correctly