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Following injury to the central nervous system, mitochondrial dysfunction and generation of reactive oxygen species could lead to activation of neuronal and glial cell apoptosis [6], [42], [43]

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A 1:1 matching on propensity score ( 0.02) of subjects treated with ALCAR 3 g/day with not treated subjects, and, separately, of subjects treated with ALCAR 1.5 g/day with not treated subjects, was then performed using the same pool of not treated subjects

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