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Proton magnetic resonance spectroscopy in subjects with high genetic risk of schizophrenia: Investigation of anterior cingulate, dorsolateral prefrontal cortex and thalamus

Cited 61 time in Web of Science Cited 64 time in Scopus
Authors

Yoo, So Young; Yeon, Suran; Choi, Chi-Hoon; Kang, Do-Hyung; Shin, Na Young; Choi, Jung-Seok; Kwon, Jun Soo; Jang, Dong-Pyo; Jung, Wi Hoon; Lee, Jong-Min

Issue Date
2009-06
Publisher
ELSEVIER SCIENCE BV
Citation
SCHIZOPHRENIA RESEARCH; Vol.111, Issues 1-3; 86-93
Keywords
Magnetic resonance spectroscopyHigh genetic riskSchizophrenia
Abstract
Objective: Reduced N-acetylaspartate levels in regions of the frontal cortex, including the anterior cingulate cortex, dorsolaterail prefrontal cortex, and thalamus, involved in the pathophysiology of schizophrenia suggest that brain metabolite abnormalities may be a marker of genetic vulnerability to schizophrenia. We used proton magnetic resonance spectroscopy (H-MRS) to acquire absolute concentrations of brain metabolites in subjects with a high genetic risk of schizophrenia to investigate the potential relationship between unexpressed genetic liability to schizophrenia and neuronal dysfunction. Method: Included in the study were 22 subjects who had at least two relatives with schizophrenia (high genetic risk group) and 22 controls with no second-degree relatives with schizophrenia. Absolute concentrations of N-acetylaspartate, creatine, choline, glutamate/glutamine, and myo-inositol and the ratios of metabolites in the anterior cingulate cortex, left dorsolateral prefrontal cortex, and left thalamus were measured using H-MRS at 1.5 Tesla. Results: Relative to the controls, the high genetic risk group showed significant differences in absolute metabolite levels in the spectra of the regions of the left thalamus, including significant decreases in N-acetylaspartate, creatine, and choline concentrations. Conclusions: The study points to neuronal dysfunction, and in particular thalamic dysfunction, as a key region of the vulnerability marker of schizophrenia. Further studies should examine the nature of the thalamus more intensively to further our understanding of thalamic dysfunction as a vulnerability marker.
ISSN
0920-9964
Language
English
URI
https://hdl.handle.net/10371/78564
DOI
https://doi.org/10.1016/j.schres.2009.03.036
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