Abstract #3564
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
1
Russell H. Morgan Department of Radiology
and Radiological Science, Johns Hopkins University
School of Medicine, Baltimore, Maryland, United States,
2
Department
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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