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In the brain, where neurons have limited capacity to break down FFAs, lipids are continuously shuttled to astrocytes via ApoE [43]

An increase in the renal production of ammonia could be another factor that contributes to the development of hyperammonaemia in VPA-treated patients

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Hyperammonemia is due to acetyl coenzyme A (CoA) decrease and inhibition of NAGS and CPS1 activities22 by toxic metabolites