Abstract
Abnormalities in glutamate neurotransmission are linked to psychotic symptoms and cognitive dysfunction in schizophrenia. magnetic resonance spectroscopy (MRS) provides an acceptable means of measuring glutamate in the human brain but findings from patient studies at conventional magnetic field strength show considerable heterogeneity. Ultra-high-field MRS offers greater precision in glutamate measurement, particularly in delineation of glutamate from its precursor and metabolite, glutamine. This study aimed to use high-field (7 T) MRS to measure concentrations of glutamate and glutamine in three brain regions, anterior cingulate cortex (ACC), dorsolateral prefrontal cortex (DLPFC) and putamen (PUT), in young men with early psychosis. MRS was performed in 17 male participants with early psychosis and 18 healthy age-matched controls. Neurometabolite levels were calculated with unsuppressed water signal as the reference and corrected for individual grey matter, white matter and cerebrospinal fluid concentration. Cognitive function was measured with the Brief Assessment of Cognition in Schizophrenia (BACS). Compared to controls, patients with early psychosis had lower concentrations of glutamate and glutamine in ACC. No differences were apparent in the DLPFC and PUT. In patients with early psychosis, there was a highly significant correlation between glutamate concentration in ACC and performance on the BACS, though the numbers available for this analysis were small. Our finding of lower glutamate levels in ACC in patients with schizophrenia is consistent with a recent meta-analysis of 7 T studies and suggests that this abnormality is present in both patients with early psychosis and those with longer-established illness. The possible link between ACC glutamate and cognitive performance requires replication in larger studies.
Highlights
The role of glutamate neurons in the pathophysiology of schizophrenia is attracting intense research interest [1,2,]
In patients with schizophrenia, glutamate levels were increased in basal ganglia while levels of glutamine were elevated in thalamus
Participants with psychosis were recruited through Early Intervention in Psychosis service, Oxford Health NHS Foundation Trust, and Department of Psychosis Studies, Institute of Psychiatry, London, from patients diagnosed with early psychosis by their treating psychiatrist, independent of the research team, according to the Diagnostic and Statistical Manual for Mental Disorders Fifth Edition (DSM-5) criteria [12]
Summary
The role of glutamate neurons in the pathophysiology of schizophrenia is attracting intense research interest [1,2,]. A meta-analysis of 59 case–control studies (1686 patients and 1451 healthy controls) found no difference between patients with schizophrenia and controls in glutamate and glutamine levels in frontal brain regions [3]. In patients with schizophrenia, glutamate levels were increased in basal ganglia while levels of glutamine were elevated in thalamus. These findings suggest that the impact of schizophrenia on brain glutamate activity may show distinct regional specificity. It has been suggested that abnormalities in glutamate might alter during the course of the illness with elevated levels being apparent at onset of psychosis, while lower levels supervene in patients with more established illness [4]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
