Aromatic L-amino acid decarboxylase (AADC) deficiency is a rare autosomal recessive disease that causes defective synthesis of dopamine and serotonin, and children with AADC deficiency exhibit severe motor, behavioral and autonomic dysfunctions. We have created an IVS6+4A>T knock-in mouse model of AADC (DdcKI mice) and shown that gene therapy at the neonatal stage can rescue the phenotype. In this study, we extended the treatment to systemic therapy on young mice. After intraperitoneal injection of 7-day-old mice with either AAV9-CMV-hAADC (AAV9-AADC) or yfAAV9/3-Syn-I-mAADC (AAVN-AADC), the treated DdcKI mice showed improvements in weight gain, survival, motor function, autonomic function, and behavior, but the effects of AAVN-AADC were superior. The survival of AAVN-AADC treated DdcKI mice (95%) was slightly better than that of the AAV9-AADC treated mice (78%), but this difference was not significant. Brain AADC activity of both AAV9-AADC and AAVN-AADC treated mice was slightly elevated (2.3% and 2.7% of wild-type, respectively). Untreated DdcKI mice had difficulties maintaining body temperature during cold exposure, and both AAV9-AADC- and AAVN-AADC-treated DdcKI mice exhibited body temperature control similar to that of WT mice in cold environments. Moreover, the AAV9-AADC-treated DdcKI mice exhibited slight hyperactivity. Under low magnification, AADC-positive cells were found in the cortex of AAV9-AADC-treated mice. Therefore, mice with a neurotransmitter deficiency can be rescued at a young age using systemic gene therapy, but a neuron-specific vector may be necessary.