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Koeller DM et al (2002) Biochemical, pathologic and behavioral analysis of a mouse model of glutaric acidemia type I

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Others, by contrast, report reductions in mitochondrial ATP production following LCAC treatment, as well as acute increases in mitochondrial reactive oxygen species (Piper et al., 1984

The compound also decreased the activity of stress-induced kinases (SAPK/JNK and pERK1/2), suggesting additional neuroprotective mechanisms beyond simple neurotrophin upregulation