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Thus, to illustrate these combining points (i.e., [13, 44, 63]), considering that white matter injury is the major cause of functional loss after SCI [45, 52], it is important to note that cysts and the loss of axons instead of hemorrhagic areas were observed in the white matter in all of the controls beginning on day 7 and that the rats exhibited a tail motor score that persisted with only small improvements, sustained debilitation, sustained tail spasticity until the end of the experiment (day 360), a decrease in the number of large myelinated axons in the caudal nerve, a higher MUP (giant potential) in the tail muscle, and a group of atrophic fibers that likely represented a large unit that acquired many fibers through collateral reinnervation and then degenerated

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To make the current evidence and gaps explicit, we now include Table 2 summarizing representative ferroptosis-in-AD studies (human, animal, and cellular), indicating which hallmarks were examined and whether selective rescue or checkpoint linkage was established (Bao et al., 2021

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