Roy H. Perlis

This study uses CRISPR screening to identify schizophrenia-associated genes that regulate microglial phagocytosis and morphology, revealing potential therapeutic targets.

This paper identifies a brain-enriched circRNA in blood that predicts response to SSRI antidepressants and is regulated by 5-HT2A and BDNF signaling.

This study shows that atypical antipsychotics like clozapine and olanzapine alter microglial functions through astrocyte-derived extracellular vesicles by affecting phagocytosis and motility.

The paper screens CNS-penetrant compounds to identify small molecules that modulate microglial phagocytosis of synaptosomes, finding 28 compounds with significant effects.

The paper shows that Hofbauer cells and fetal brain microglia share transcriptional profiles and responses to maternal diet-induced obesity, suggesting Hofbauer cells as a noninvasive biomarker for fetal microglial programming.

This study uses EHR data to estimate TRD probability and identifies two genome-wide significant loci linked to metabolic traits, suggesting shared biology with related conditions.

This study shows that knocking out CYFIP1 in human microglia reduces synaptic vesicle phagocytosis, morphology changes, and motility, suggesting a role in synaptic pruning related to neurodevelopmental disorders.

This study shows SARS-CoV-2 infection in human brain organoids leads to microglial synapse elimination, linking it to potential cognitive impairments post-COVID-19.

This study identifies molecular and functional changes in mouse and human models of 16p11.2 reciprocal genomic disorder, revealing context-specific disruptions in energy metabolism, RNA processing, and neuronal development.

This study investigates how the 22q11.2 deletion affects gene expression in neural progenitor cells and neurons, linking it to schizophrenia risk through altered presynaptic gene products.

The paper shows that increasing neuronal activity in human cerebral spheroids increases new neurons and decreases new glial cells, with reduced miR-135a expression.

The paper examines the relationship between white matter hyperintensity burden, resting state functional connectivity, and cognitive functions in older adults, finding associations with memory retrieval but not other cognitive tasks.

The paper uses single-cell RNA sequencing to compare fetal brain microglia and Hofbauer cells, revealing shared transcriptional programs and sex-specific differences.

This paper develops a transcriptome-based polygenic risk score (T-PRS) linking depression-related cortical gene expression changes to brain morphology and symptom severity in MDD.

The paper develops a model to identify patients likely to have a genetic disease using EHR data, achieving high accuracy in predicting genetic testing needs.

This study generates patient-derived microglia-like cells from umbilical cord blood to model fetal brain immune responses to maternal SARS-CoV-2 exposure.

This study shows n-3 PUFAs promote astrocyte differentiation and increase neurotrophin production in patient-derived neural stem cells, independent of cAMP and dependent on CREB.

This paper shows that GWAS using minimal phenotyping for depression identifies non-specific genetic factors shared with other psychiatric conditions, not specific to major depressive disorder.

The study finds that rare copy number variants (CNVs) contribute to bipolar disorder risk primarily in schizoaffective disorder bipolar type cases, with differences in CNV burden and schizophrenia polygenic risk scores between subtypes.

This paper conducts a meta-analysis showing that CYP2C19 poor metabolizers have better antidepressant efficacy but similar side effects compared to extensive metabolizers.

This paper validates EHR-based BD phenotyping algorithms by showing their genetic correlation with traditional BD cases, suggesting they identify genetically similar cases.

The paper shows increased microglial synapse elimination in schizophrenia patient models and links it to genetic variants and potential therapeutic interventions.

This study identifies two SNPs associated with antidepressant response in GENDEP and STAR*D studies but finds limited replication in independent cohorts.

This study investigates whether polygenic risk scores (PRS) can predict antidepressant response in MDD, finding no significant predictive effect.