Zohreh Farsi

The paper uses spatial omics to analyze translational dysregulation in Grin2a+/- mice, finding gene-specific translation reductions in neurons and non-neuronal cells linked to schizophrenia pathophysiology.

This study investigates Akap11 mutant mice to explore the neurobiological effects of AKAP11 loss, finding increased PKA activity and transcriptomic changes linked to schizophrenia and bipolar disorder.

This study examines the effects of Grin2a and Akap11 mutations on striatal dopamine dynamics and behavior in mice, revealing distinct impacts on locomotion and neural activity.

This study performs a meta-analysis of brain transcriptomes from genetic mouse models of schizophrenia, identifying dysregulation in striatum and thalamus with distinct patterns in different models.

This study examines Gria3 mutant mice to identify transcriptomic and proteomic changes linked to schizophrenia, finding region-specific gene dysregulation and synaptic protein alterations.

This study uses multi-omics analyses of Sp4 mutant mice to reveal synapse disruption and age- and region-specific neuronal and glial changes linked to schizophrenia and bipolar disorder.

This study shows that SRRM2 haploinsufficiency in mice causes synaptic, splicing, and myelination defects linked to schizophrenia-like behaviors and gene expression changes.

This study investigates how different GRIN2A mutations linked to schizophrenia, epilepsy, and developmental disorders affect NMDA receptor function, revealing distinct functional consequences.

The paper shows that Cdr1as regulates miR-7 activity, which controls glutamatergic transmission and neuronal connectivity in forebrain neurons.

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 examines EEG abnormalities in Grin2a and Akap11 mutant mice, finding similarities with schizophrenia patients, suggesting these mutants as models for the disorder.