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This neurotrophic effect of OA is mediated through the activation of peroxisome proliferator-activated receptor-alpha (PPAR), as evidenced by the diminished neuronal differentiation observed when PPAR is silenced (Fig

Sphingolipid Metabolism Is Dysregulated at Transcriptomic and Metabolic Levels in the Spinal Cord of an Animal Model of Amyotrophic Lateral Sclerosis

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Collectively, these innovations hold the potential to reduce required sample sizes, shorten trial durations, and improve statistical power, thus addressing some of the most persistent limitations in the development and validation of neuroprotective therapies [610]