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While AE1 is progressively phosphorylated in response to oxidative stress when parasites transition from the ring to schizont stage (Pantaleo et al., 2010), the resulting reduction in AE1 affinity for the cytoskeleton and consequential membrane destabilization occur at the end of the cell cycle (Ferru et al., 2011), which is more consistent with a role in merozoite egress rather than NPP function

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Notably, as suggested in an animal model of neuroinflammation induced by ischemic stroke damage known to increase the prevalence of M1 microglia in the brain, pre-treatment with melatonin upregulated the expression of TREM2 while downregulating that of proinflammatory genes in microglia (e.g., inducible nitric oxide synthase) [101], suggesting that melatonin may polarize microglia towards its M2 phenotype