Kynurenine pathway dysregulation in attention-deficit hyperactivity disorder: Impact on N-methyl-D-aspartate receptors and phasic dopamine maturation

Figure 3 The “metabolic detour”: Selective kynurenine pathway modulation to restore network coordination. A diagrammatic representation of the therapeutic potential of kynurenine 3-monooxygenase inhibitors in attention-deficit/hyperactivity disorder. Unlike stimulants that act on neurotransmitter transporters, kynurenine 3-monooxygenase inhibitors correct metabolic “noise” by preventing the accumulation of N-methyl-D-aspartate-agonistic neurotoxins. The resulting increase in the “neuroprotective buffer” (kynurenic acid) facilitates bottom-up stabilization of biological rhythms and network coordination, offering a precision-medicine approach for patients who are refractory to standard stimulant treatments. ADHD: Attention-deficit/hyperactivity disorder; DAT: Dopamine transporter; KMO: Kynurenine 3-monooxygenase; KP: Kynurenine pathway.