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Figure 2 | Journal of Neuroinflammation

Figure 2

From: Absence of the complement regulatory molecule CD59a leads to exacerbated neuropathology after traumatic brain injury in mice

Figure 2

Serum levels of neuron-specific enolase (NSE), a marker of neuronal cell death. NSE protein levels were quantified in serum samples by ELISA, as described in the methods section. In sham-operated wild-type and CD59a-/- mice, NSE was not detectable in any sample at any time-point, i.e. below the sensitivity of the assay at 1 pg/ml. In contrast, NSE serum levels were significantly elevated at 4 h and 24 h after trauma, both in wild-type and CD59a-/- mice, compared to sham-operated controls. In addition, the NSE serum levels were significantly higher at both time-points in head-injured CD59a-/- mice, compared to wild-type littermates (*P < 0.05 for t = 4 h, **P < 0.05 for t = 24 h). This implies a greater extent of neuronal cell death in the genetic absence of Cd59a. NSE was not detectable in head-injured mice at 7 days. Data are shown as mean ± SEM for n = 3 per group and time-point. TBI, traumatic brain injury; WT, wild-type.

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