Abnormal neurobiochemical metabolites in the first
10.11817/j.issn.1672-7347.2021.200240
- Author:
Lijun OUYANG
1
,
2
,
3
,
4
,
5
;
Wenxiao ZHENG
1
,
2
,
3
,
4
,
6
;
Xiaoqian MA
1
,
2
,
3
,
4
,
6
;
Liu YUAN
1
,
2
,
3
,
4
,
6
;
Ying HE
1
,
2
,
3
,
4
,
7
;
Xiaogang CHEN
1
,
2
,
3
,
4
,
8
Author Information
1. Mental Health Institute, Second Xiangya Hospital, Central South University
2. China National Technology Institute on Mental Disorders
3. National Technology Institute on Mental Disorders
4. Hunan Key Laboratory of Psychiatry and Mental Health
5. Hunan Medical Center for Mental Health, Changsha 410011, China. lijunouyang@csu.edu.cn.
6. Hunan Medical Center for Mental Health, Changsha 410011, China.
7. Hunan Medical Center for Mental Health, Changsha 410011, China. yinghe@csu.edu.cn.
8. Hunan Medical Center for Mental Health, Changsha 410011, China. Chenxiaogang@csu.edu.cn.
- Publication Type:Journal Article
- Keywords:
first-episode schizophrenia;
high-risk population;
magnetic resonance spectroscopy
- MeSH:
Aspartic Acid;
Glutamic Acid;
Glutamine;
Humans;
Magnetic Resonance Imaging;
Magnetic Resonance Spectroscopy;
Proton Magnetic Resonance Spectroscopy;
Schizophrenia
- From:
Journal of Central South University(Medical Sciences)
2021;46(10):1090-1095
- CountryChina
- Language:English
-
Abstract:
OBJECTIVES:To explore the metabolite characteristics in medial prefrontal cortex (mPFC) by
METHODS:A total of 46 patients with the first-episode schizophrenia (FES), 49 people with clinical high risk (CHR), 61 people with genetic high risk (GHR), and 58 healthy controls (HC) were enrolled. The levels of N-acetylaspartylglutamate+N-acetylaspartate (tNAA), choline-containing compounds (Cho) and myo-inositol (MI), glutamate+glutamine (Glx) in medial prefrontal cortex were measured by single-voxel
RESULTS:There were significant differences in Glx, tNAA, and MI concentrations among 4 groups (all
CONCLUSIONS:The decreased levels of MI and Glx in the FES patients suggest that there may be glial functional damage and glutamatergic transmitter dysfunction in the early stage of the disease. The compensatory increase of metabolites may be a protective factor for schizophrenia in the genetic individuals.
