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H 2 O 2 levels rise during surges of peroxisomal β-oxidation (e.g., fasting or PPARα activation), ether-lipid (plasmalogen) synthesis and polyamine detoxification via amine oxidases

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The pathophysiological molecular mechanisms underlying cognitive dysfunction caused by TBI are complex and primarily involve central nervous system inflammation, oxidative stress, free radical damage and disrupted metabolism of neuroprotective factors [117]