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10.3389/fphar.2021.680674 36 HutchinsonM

This could be because of complement C1q/C3 tagging at the synapse, neuronal "eat-me" signals such as phosphatidylserine recognised by microglial TREM2/MERTK, or simply because presynaptic terminals (at the small axon boutons) are more accessible to microglia than the larger postsynaptic dendrites [94, 95]

45 It appears that genotypic changes of these enzymes leads to potentially different risk/benefit ratios when APAP is ingested

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Ferroptosis is involved in the development of neuropathic pain and allodynia