Open AccessN-Acetylaspartylglutamate (NAAG) and N-Acetylaspartate (NAA) in Patients With Schizophrenia
Author(s) -
Frank Jessen,
Natascha Fingerhut,
Alois M. Sprinkart,
KaiUwe Kühn,
Nadine Petrovsky,
Wolfgang Maier,
H. H. Schild,
Wolfgang Block,
Michael Wagner,
Frank Träber
Publication year - 2011
Publication title -
schizophrenia bulletin
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.823
H-Index - 190
eISSN - 1745-1701
pISSN - 0586-7614
DOI - 10.1093/schbul/sbr127
Subject(s) - glutamate receptor , schizophrenia (object oriented programming) , glutamatergic , prefrontal cortex , medicine , psychology , glutamate carboxypeptidase ii , neuroscience , endocrinology , anterior cingulate cortex , receptor , psychiatry , cognition , prostate , cancer
BACKGROUND : Imbalance of glutamatergic neurotransmission has been proposed as a key mechanism underlying symptoms of schizophrenia. The neuropetide N-acetylaspartylglutamate (NAAG) modulates glutamate release. NAAG provides a component of the proton magnetic resonance spectrum (1H-MRS) in humans. The signal of NAAG, however, largely overlaps with its precursor and degrading product N-acetylaspartate (NAA) that by itself does not act in glutamatergic neurotransmission.
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