Evidence for the role of NMDA receptor hypofunction in schizophrenia comes from pharmacological studies of phencyclidine and ketamine. These NMDA receptor antagonists have shown to produce schizophrenia-like behaviors in rodents ; to induce positive and negative symptoms in healthy humans ; and to aggravate psychotic symptoms in patients with schizophrenia. Glutamate also plays a role in synaptic plasticity via NMDA receptors mediating higher cognitive functions such as learning and memory. NMDA receptor dysfunction has also been implicated in the cognitive deficits of schizophrenia. In these people, agents that enhance NMDA receptor activity have shown to improve negative symptoms and to facilitate memory consolidation. The brain areas associated with NMDA receptor hypofunction in schizophrenia include the Minoxidil prefrontal cortex and hippocampus. The relationship between NMDA receptor hypofunction and glutamate release is not fully understood. NMDA hypofunction in schizophrenia could be related to insufficient or excessive glutamate release which may also differ between brain regions. Increased glutamate Levocetirizine dihydrochloride exposure and its duration could explain the psychotoxic effects in schizophrenia. Proton Magnetic Resonance Spectroscopy is a feasible method for in vivo quantification of glutamate concentration and other brain metabolites that, if altered, may reflect abnormal neuro-developmental features. In schizophrenia an increasing number of 1H-MRS studies have been conducted. Although inconclusive, 1H-MRS findings also suggest abnormal glutamatergic neurotransmission. Furthermore, we assessed levels of plasma proline and plasma glutamine in the 22q11DS group. Increased proline has been reported in 22q11DS patients. In children with 22q11DS there was a relationship between increased plasma proline and decreased brain function. High levels of proline in 22q11DS, consequence of POX deficiency, may be related to glutamate dysfunction particularly in 22q11DS SCZ+. Hence, we expected that plasma proline will be increased in 22q11DS SCZ+ and that it will correlate with glutamate concentrations in the brain.