Schizophrenia research and treatment

This study identifies modifiable comorbidities of schizophrenia by analyzing EHR data and polygenic risk scores, finding conditions with no shared genetic risk that may be influenced by treatment or environment.

The paper investigates cyclophilin D (CypD) alterations in parvalbumin interneurons (PVIs) in schizophrenia, linking CypD to redox dysregulation and PVI dysfunction.

This paper investigates dopamine release mode abnormalities in a schizophrenia-like model and identifies mechanisms involving serotonergic regulation and antipsychotic effects.

The paper uses brain cell-type-specific protein interactomes to interpret genetic data in schizophrenia and identifies enriched networks and genes associated with the disease.

The paper shows that non-additive effects of schizophrenia risk genes are due to convergent downstream transcriptomic effects and sub-additive changes, suggesting functional redundancy as a mechanism for non-additivity.

This study examines Slc10a4 knockout mice to assess their role in auditory processing and sensory motor gating, suggesting they may model neuropsychiatric disorders like schizophrenia.

This study shows that activating prefrontal parvalbumin interneurons improves working memory deficits in a mouse model of schizophrenia, even when mice are continuously treated with antipsychotics.

This study uses 7-Tesla MRS to track longitudinal changes in brain metabolites in FEP patients and healthy controls, identifying potential trait and state markers for psychosis.

This study investigates how optogenetic stimulation of parvalbumin-positive interneurons in the prefrontal cortex and ventral hippocampus can rescue cognitive inflexibility induced by dizocilpine in rats.

This study examines brain morphometric deviations in individuals at clinical high-risk for psychosis and finds they largely overlap with healthy variation and are not strongly associated with symptom severity or conversion to psychosis.

This study investigates the neural mechanisms of cognitive impairment in a schizophrenia mouse model and shows that risperidone rescues memory and auditory perception deficits by restoring mPFC-dHPC connectivity.

This study shows that chronic dopamine transporter blockade in the mouse hippocampus causes learning and memory deficits, which are partially reversed by D2 receptor antagonists.

The paper identifies eight drug candidates for repurposing to treat cognitive symptoms in schizophrenia, with sex-specific recommendations based on gene expression differences.

This study shows that GluA1 dysfunction leads to impaired short-term habituation, resulting in a hyper-dopaminergic phenotype in the nucleus accumbens, which may contribute to aberrant salience in schizophrenia.

This study identifies shared genetic and biological mechanisms between schizophrenia, bipolar disorder, and type 2 diabetes mellitus using integrative analysis of gene expression datasets.

This paper reviews genomic studies and iPSC-based models of schizophrenia to summarize current progress in understanding its genetic basis and cellular mechanisms.

This study identifies brain region-specific changes and dopamine dysregulation in Grin2a mutant mice, supporting schizophrenia hypotheses and highlighting their utility as a genetic model.

This study shows that selectively increasing dopamine in the dorsal striatum impairs behaviors linked to negative and cognitive symptoms of psychosis, challenging the idea that excess dopamine is not involved in these symptoms.

This study identifies the miR-124-AMPAR pathway as a common mediator linking polygenic risks to shared behavioral changes in schizophrenia and bipolar disorder.

This study finds that individuals at clinical high risk for psychosis have larger choroid plexus volumes, associated with neuroanatomical changes and plasma analyte markers.

The paper identifies selective vulnerability of supragranular layer neurons in schizophrenia through single nucleus RNA sequencing and histological analysis.

The paper identifies sex differences in schizophrenia across three brain regions using RNA-seq and genotypes, finding sex-specific genes, eQTLs, and transcriptional features.

This study links schizophrenia polygenic risk to cortical thickness changes in developing children, showing a trajectory toward adult schizophrenia patterns.

The paper introduces a framework to identify individual-specific biopsychosocial fingerprints for neuropsychiatric disorders using affinity scores, achieving high classification accuracy.

The paper identifies Egr3-dependent genes in mice hippocampi after ECS, finding genes related to DNA damage response and schizophrenia.

This study calculates pathway-based polygenic risk scores for schizophrenia using gene-sets related to synaptic function and histone modification, and finds associations with neuroimaging and clinical traits in UK Biobank.

This study finds that higher positive schizotypal traits are linked to reduced somatosensory attenuation and precision for self-generated touch.

The paper examines UK Biobank participants with protein truncating variants in schizophrenia-associated genes, finding limited psychiatric symptoms despite increased risk.