Despite these links between genetic risk and neural alterations, and the supporting evidence of causal involvement provided by rodent studies, a dearth of information exists regarding molecular disruptions in these brain regions in OCD. To address this knowledge gap, we recently examined a targeted list of excitatory- and inhibitory-synapse-related transcripts in the OFC, caudate, and nucleus accumbens in OCD post-mortem brain tissue. This analysis demonstrated lower excitatory synapse-related transcripts in OCD subjects in both OFC and striatum, though reductions were more pronounced in the OFC36. However, this initial study only looked at a small subset of transcripts and therefore could not paint a complete picture of possible OFC and striatal dysfunction. Another recent study used unbiased RNA-sequencing (RNAseq) to identify gene expression differences in striatal subregions (caudate, putamen, and nucleus accumbens) of OCD subjects compared to unaffected comparison subjects, and observed differences in gene expression between striatal subregions. Genes that were differentially expressed between OCD subjects and unaffected comparison subjects in this study were also enriched for synaptic and immune function protein-encoding transcripts37. However, this study only examined the striatum
