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Flux of glutamate out of the glutathione cycle may also lead to compensatory changes in activity or protein expression of glutathione cycle enzymes or transmembrane transporters that supply substrates to the pathway

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Proposed mechanisms include: Persistent immune dysregulation Metabolic changes Central sensitization and altered pain processing Residual tissue injury Autonomic dysfunction Psychological and behavioral contributors The controversial possibility of persistent Borrelia organisms or bacterial remnants The authors advocate using an inclusive classification for persistent symptoms attributed to Lyme disease while acknowledging that the exact cause may differ among patients