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

TL;DR: This study proposes a mechanistic model explaining persisting disability in schizophrenia, attributing it to imprecise predictive coding via cortico-striatal-thalamo-cortical loop dysfunction, which is linked to early classical symptoms and reality distortion, and has implications for novel treatment development.

TL;DR: A meta-analysis of 1H-MRS studies comparing levels of Glu-and its metabolites in the brains of TRS and non-treatment resistant schizophrenia (nTRS) patients found the higher ACC Glu in TRS was not associated with symptom severity or antipsychotic administration, indicating a possible trait abnormality.

TL;DR: TRS is poorly studied and understood condition contrasted to its high prevalence, clinical importance and poor prognosis, and there is a lack of studies on epidemiology, for example risk factors and predictors of outcome in TRS.

TL;DR: The present study sought to examine potential mediating and moderating factors underlying the complex relationship between childhood adversity and schizophrenia and whether the effect of childhood adversity on IQ is influenced by brain volume or genetic variation and if so, how these factors differ between patients with and without treatment-resistant schizophrenia.

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.