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Article: In vivo gamma-aminobutyric acid and glutamate levels in people with first-episode schizophrenia: A proton magnetic resonance spectroscopy study

TitleIn vivo gamma-aminobutyric acid and glutamate levels in people with first-episode schizophrenia: A proton magnetic resonance spectroscopy study
Authors
KeywordsGamma-aminobutyric acid
Glutamate
First-episode schizophrenia
Proton magnetic resonance spectroscopy
Biomarker
Anterior cingulate cortex
Issue Date2018
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/schres
Citation
Schizophrenia Research, 2018, v. 193, p. 295-303 How to Cite?
AbstractBackground: Gamma-aminobutyric acid (GABA) dysfunction and its consequent imbalance are implicated in the pathophysiology of schizophrenia. Reduced GABA production would lead to a disinhibition of glutamatergic neurons and subsequently cause a disruption of the modulation between GABAergic interneurons and glutamatergic neurons. In this study, levels of GABA, Glx (summation of glutamate and glutamine), and other metabolites in the anterior cingulate cortex were measured and compared between first-episode schizophrenia subjects and healthy controls (HC). Diagnostic potential of GABA and Glx as upstream biomarkers for schizophrenia was explored. Methods: Nineteen first-episode schizophrenia subjects and fourteen HC participated in this study. Severity of clinical symptoms of patients was measured with Positive and Negative Syndrome Scale (PANSS). Metabolites were measured using proton magnetic resonance spectroscopy, and quantified using internal water as reference. Results: First-episode schizophrenia subjects revealed reduced GABA and myo-inositol (mI), and increased Glx and choline (Cho), compared to HC. No significant correlation was found between metabolite levels and PANSS scores. Receiver operator characteristics analyses showed Glx had higher sensitivity and specificity (84.2%, 92.9%) compared to GABA (73.7%, 64.3%) for differentiating schizophrenia patients from HC. Combined model of both GABA and Glx revealed the best sensitivity and specificity (89.5%, 100%). Conclusion: This study simultaneously showed reduction in GABA and elevation in Glx in first-episode schizophrenia subjects, and this might provide insights on explaining the disruption of modulation between GABAergic interneurons and glutamatergic neurons. Elevated Cho might indicate increased membrane turnover; whereas reduced mI might reflect dysfunction of the signal transduction pathway. In vivo Glx and GABA revealed their diagnostic potential for schizophrenia.
Persistent Identifierhttp://hdl.handle.net/10722/246061
ISSN
2023 Impact Factor: 3.6
2023 SCImago Journal Rankings: 1.374
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChiu, PW-
dc.contributor.authorLui, SSY-
dc.contributor.authorHung, KSY-
dc.contributor.authorChan, RCK-
dc.contributor.authorChan, Q-
dc.contributor.authorSham, PC-
dc.contributor.authorCheung, EFC-
dc.contributor.authorMak, HKF-
dc.date.accessioned2017-09-18T02:21:43Z-
dc.date.available2017-09-18T02:21:43Z-
dc.date.issued2018-
dc.identifier.citationSchizophrenia Research, 2018, v. 193, p. 295-303-
dc.identifier.issn0920-9964-
dc.identifier.urihttp://hdl.handle.net/10722/246061-
dc.description.abstractBackground: Gamma-aminobutyric acid (GABA) dysfunction and its consequent imbalance are implicated in the pathophysiology of schizophrenia. Reduced GABA production would lead to a disinhibition of glutamatergic neurons and subsequently cause a disruption of the modulation between GABAergic interneurons and glutamatergic neurons. In this study, levels of GABA, Glx (summation of glutamate and glutamine), and other metabolites in the anterior cingulate cortex were measured and compared between first-episode schizophrenia subjects and healthy controls (HC). Diagnostic potential of GABA and Glx as upstream biomarkers for schizophrenia was explored. Methods: Nineteen first-episode schizophrenia subjects and fourteen HC participated in this study. Severity of clinical symptoms of patients was measured with Positive and Negative Syndrome Scale (PANSS). Metabolites were measured using proton magnetic resonance spectroscopy, and quantified using internal water as reference. Results: First-episode schizophrenia subjects revealed reduced GABA and myo-inositol (mI), and increased Glx and choline (Cho), compared to HC. No significant correlation was found between metabolite levels and PANSS scores. Receiver operator characteristics analyses showed Glx had higher sensitivity and specificity (84.2%, 92.9%) compared to GABA (73.7%, 64.3%) for differentiating schizophrenia patients from HC. Combined model of both GABA and Glx revealed the best sensitivity and specificity (89.5%, 100%). Conclusion: This study simultaneously showed reduction in GABA and elevation in Glx in first-episode schizophrenia subjects, and this might provide insights on explaining the disruption of modulation between GABAergic interneurons and glutamatergic neurons. Elevated Cho might indicate increased membrane turnover; whereas reduced mI might reflect dysfunction of the signal transduction pathway. In vivo Glx and GABA revealed their diagnostic potential for schizophrenia.-
dc.languageeng-
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/schres-
dc.relation.ispartofSchizophrenia Research-
dc.subjectGamma-aminobutyric acid-
dc.subjectGlutamate-
dc.subjectFirst-episode schizophrenia-
dc.subjectProton magnetic resonance spectroscopy-
dc.subjectBiomarker-
dc.subjectAnterior cingulate cortex-
dc.titleIn vivo gamma-aminobutyric acid and glutamate levels in people with first-episode schizophrenia: A proton magnetic resonance spectroscopy study-
dc.typeArticle-
dc.identifier.emailChiu, PW: pwcchiu@hku.hk-
dc.identifier.emailLui, SSY: lsy570@hku.hk-
dc.identifier.emailSham, PC: pcsham@hku.hk-
dc.identifier.emailMak, HKF: makkf@hku.hk-
dc.identifier.authorityLui, SSY=rp02747-
dc.identifier.authoritySham, PC=rp00459-
dc.identifier.authorityMak, HKF=rp00533-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.schres.2017.07.021-
dc.identifier.pmid28751130-
dc.identifier.scopuseid_2-s2.0-85025805318-
dc.identifier.hkuros276882-
dc.identifier.volume193-
dc.identifier.spage295-
dc.identifier.epage303-
dc.identifier.isiWOS:000427784100047-
dc.publisher.placeNetherlands-
dc.identifier.issnl0920-9964-

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