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The release of excess iron during CNS demyelination is potentially directly neurotoxic due to increased extracellular concentrations of unbuffered ferrous iron in the form of divalent cations (Fe 2+ ), which amplifies oxidative injury via the Fenton reaction [171]

[5] In the same 28-day study, DIO mice showed reduced body weight and fat mass gains alongside improved glucose tolerance and attenuated hepatic steatosis

171 In our previous study, we reported that the expression of AQP4 was decreased by exposure to CUMS, which contributed to dysfunction of glymphatic circulation and depressive-like behaviors in mice