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One article proposed that excessive serotonin levels could explain classic symptoms of ME/CFS (433), as it would promote the release of excess CRH, and therefore cause chronic reactivation of the HPA axis (434)

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In the review, we highlight recent advancements in our understanding of how UA exerts neuroprotective effects on neurodegenerative diseases and emphasize the dual roles of UA in managing oxidative stress and neuroinflammation