Attention deficit hyperactivity disorder (ADHD) is a long recognized and common childhood disorder. ADHD adolescents
tend to encounter more difficulties in school and peer relationships, whereas ADHD adults have more occupational and interpersonal difficulties.
However, with the treatment of central nervous system (CNS) stimulants, 10-20 % of the patients still remain poor responders to
treatment. Among hypotheses for ADHD, dysfunction of N-methyl-D-aspartate (NMDA)-type glutamate receptors has recently been
suggested by accumulating genetic and animal studies. This article systemically reviews evidence supporting NMDA dysfunction as a
potential ADHD pathogenesis from perspectives of neurodevelopment, attentional circuitry, and impulse inhibition. The review also addresses
the development of novel treatments for ADHD via modulation of glutamatergic system, particularly the NMDA/glycine site.
These so-called NMDA enhancers may provide a new treatment option for patients with ADHD.