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In APP/PS1 mice, BBB permeability and pericyte number are reduced, and -amyloid induces mitochondrial autophagy-dependent ferroptosis via the CD36/PINK/PARKIN pathway, resulting in blood-brain barrier damage and contributing to AD

In contrast, the oxytocin metabolite OT(49) enhanced sociability in BALB/cByJ mice in a dose-dependent manner, with effects persisting up to 12 days after treatment, though without changes in repetitive behaviors [39]

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It does not typically interfere with the liver enzymes that process antibiotics, which is why there are few direct drug-to-drug interactions