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

TL;DR: The relationship between the age of onset and treatment resistant schizophrenia (TRS) is less clear as mentioned in this paper, although previous studies reported substantial heterogeneity in the relationship between TRS status and age at onset.

TL;DR: In this paper , the anterior cingulate cortex (ACC) structural subdivisions and their relationships to treatment resistance and glutamatergic levels in schizophrenia were examined in patients with treatment-resistant and clozapine-resistant schizophrenia.

TL;DR: The CLEAR (CLozapine in EARly psychosis) trial will assess whether clozapine is more effective than treatment as usual (TAU), at the level of clinical symptoms, patient rated outcomes, quality of life and cost-effectiveness in people below 25 years of age.

TL;DR: It is hypothesized that the subgroups of schizophrenia may be determined by glutamatergic and dopaminergic concentrations prior to medical treatment, and the ability to prescribe a proper medication combination, to predict the outcome in first-episode psychosis, and personalized medicine for chronic schizophrenia patients can be applied into practice.

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.