Antipsychotic treatment resistance in schizophrenia associated with elevated glutamate levels but normal dopamine function.

TL;DR: The results suggest that the focal abnormality of CC may be a potential biomarker of TRS, and a significant reduction in FA in the splenium of corpus callosum in TRS when compared to non-TRS.

TL;DR: In this article , a large sample of patients with schizophrenia, the majority of which were designated as treatment-resistant, investigated the associations between impaired insight and cortical thickness and subcortical volumes.

TL;DR: In this article , the authors examined the pathway and patterns and the impact of clozapine use in patients with TRS who were followed up for 10 years after the first outbreak of the illness.

TL;DR: In this paper , the authors used 7-Tesla magnetic resonance spectroscopic imaging (MRSI) to measure glutamate (Glu), Glutamine (Gln), and GABA from anterior and posterior regions of the insula across antipsychotic treatment.

TL;DR: The first consensus-based operational criteria for symptomatic remission in schizophrenia are based on distinct thresholds for reaching and maintaining improvement, as opposed to change criteria, allowing for alignment with traditional concepts of remission in both psychiatric and nonpsychiatric illness.

TL;DR: The locus of the largest dopaminergic abnormality in schizophrenia is presynaptic, which affects dopamine synthesis capacity, baseline synaptic dopamine levels, and dopamine release, and future drug development should focus on the control of presYNaptic dopamine synthesis and release capacity.

TL;DR: Findings indicate that dopamine overactivity predates the onset of schizophrenia in individuals with prodromal psychotic symptoms, is predominantly localized in the associative striatum, and is correlated with the severity of symptoms and neurocognitive dysfunction.

TL;DR: The tight within-patient coupling of these values, with decreased PFC activation predicting exaggerated striatal 6-fluorodopa uptake, supports the hypothesis that prefrontal cortex dysfunction may lead to dopaminergic transmission abnormalities.