Neurochem Res 40:25272543 Higgins RD, Raju T, Edwards AD, Azzopardi DV, Bose CL, Clark RH, Ferriero DM, Guillet R, Gunn AJ, Hagberg H, Hirtz D, Inder TE, Jacobs SE, Jenkins D, Juul S, Laptook AR, Lucey JF, Maze M, Palmer C, Papile L, Pfister RH, Robertson NJ, Rutherford M, Shankaran S, Silverstein FS, Soll RF, Thoresen M, Walsh WF (2011) Hypothermia and other treatment options for neonatal encephalopathy: an executive summary of the Eunice Kennedy Shriver NICHD workshop

In the female offspring, mitochondrial fusion markers on P1 suggest increased mitochondrial regeneration, while in adults increased mitochondrial fission and autophagosome markers were observed, with high levels of MnSOD and OXPHOS complex I suggesting an increase in energy demand and oxidative stress, thereby more mitochondrial turnover (Twig et al., In the developing brain, substantially high energy demand increases the need for glucose, oxygen and cerebral blood flow (Hagberg et al., Mitophagy is a crucial process to maintain mitochondrial integrity, where damaged mitochondria can be degraded and the intact components can be recycled to generate new functional mitochondria (Benard and Karbowski, Here in the newborn male SE offspring, both fission and autophagosome markers were increased without changes in the fusion marker, suggesting the mitochondrial damage by maternal SE is irreparable

6.2 Neural damage mechanisms The molecular disruptions outlined above initiate a series of cascading effects, leading to neural damage through oxidative stress, excitotoxicity, and demyelination
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