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Conversely, AR re-expression may decrease the levels of transcription factors that were initially involved in the shutdown of its expression
They suggested that minocycline may (at least in part) protect against METH-induced neurotoxicity via inhibition of microglial activation in vivo (Zhang et al., 2006)
This process generates acetyl-CoA for oxidative phosphorylation or ketone body production in the liver
Minerva Endocrinol
