N-acetyl-aspartyl-glutamate in first-episode psychosis
Anouk Marsman 1 , Subechhya Pradhan 1 , Candice Ford 2 , Ashley Lloyd 2 , Teppei Tanaka 2 , Akira Sawa 2 , and Peter B. Barker 1
Russell H. Morgan Department of Radiology
and Radiological Science, Johns Hopkins University
School of Medicine, Baltimore, Maryland, United States,
of Psychiatry, Johns Hopkins University School of
Medicine, Baltimore, Maryland, United States
The glutamatergic system plays a role in the
pathophysiology of schizophrenia.
N-acetyl-aspartyl-glutamate (NAAG) modulates this system
and may therefore be implicated in schizophrenia.
Interim analyses of an ongoing study show that patients
with first-episode psychosis show significantly (p<0.05)
lower NAAG levels and NAAG/NAA ratios in the centrum
semiovale as compared to healthy matched controls. This
could be due to altered activity of glutamate
carboxypeptidase II (GCP2), which converts NAAG into
N-acetyl-aspartate (NAA) and glutamate, and regulates
synaptic NAAG concentrations.
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