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Alpha-aminoadipate aminotransferase (AADAT) is a mitochondrial, pyridoxal phosphate-dependent enzyme that catalyzes the transamination of α-aminoadipate to glutamate in the terminal step of lysine degradation and also acts as kynurenine aminotransferase II, converting kynurenine to kynurenic acid—a neuroactive metabolite with neuroprotective properties[1][5]. AADAT is highly expressed in liver and kidney, where it supports amino acid catabolism, and also contributes to nitrogen metabolism and neurotransmitter homeostasis[1][5]. Genetic or functional alterations in AADAT have been linked to neurodevelopmental disorders (such as autism spectrum disorder), inflammatory/immune response changes, and metabolic/endocrine disturbances including thyroid hormone regulation[5]. Given its central role in amino acid and neuroactive metabolite regulation, AADAT is a potential therapeutic target in diverse pathologies involving metabolism, neurobiology, and immunity[5][3].
(For experimental inhibitors) Inhibition blocks enzymatic transamination activity, reducing formation of kynurenic acid or metabolism of lysine pathway intermediates. Modulation alters levels of kynurenine pathway metabolites that impact neuroprotection/excitation.
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