DESCRIPTION:

166 differentially expressed genes in human subjects with cocaine dependence (DSM-IV) or at least moderate cocaine use disorder (DSM-5). Subjects' peripheral blood was collected, and expression was analyzed via a genome-wide expression analysis. Microarray data available at GEO with accession number GSE116833. Data taken from Table 2. Values presented are nominal p-values.

LABEL:

Differentially expressed genes in peripheral blood mononuclear cells from cocaine use disorder patients with low and high anhedonia_p-value0.05

SCORE TYPE:

P-Value

DATE ADDED:

2021-06-21

DATE UPDATED:

2024-04-12

SPECIES:

AUTHORS:

Gabriel Rodrigo Fries, Sarwar Khan, Sydney Stamatovich, Elena Dyukova, Consuelo Walss-Bass, Scott D Lane, Joy M Schmitz, Margaret C Wardle

TITLE:

Anhedonia in cocaine use disorder is associated with inflammatory gene expression.

JOURNAL:

PloS one None 2018, Vol 13, pp. e0207231

ABSTRACT:

Treatments for Cocaine Use Disorder (CUD) are variably effective, and there are no FDA-approved medications. One approach to developing new treatments for CUD may be to investigate and target poor prognostic signs. One such sign is anhedonia (i.e. a loss of pleasure or interest in non-drug rewards), which predicts worse outcomes in existing CUD treatments. Inflammation is thought to underlie anhedonia in many other disorders, but the relationship between anhedonia and inflammation has not been investigated in CUD. Therefore, we assessed peripheral genome-wide gene expression in n = 48 individuals with CUD with high (n = 24) vs. low (n = 24) levels of anhedonia, defined by a median split of self-reported anhedonia. Our hypothesis was that individuals with high anhedonia would show differential gene expression in inflammatory pathways. No individual genes were significantly different between the low and high anhedonia groups when using t-tests with a stringent false discovery rate correction (FDR-corrected p < 0.05). However, an exploratory analysis identified 166 loci where t-tests suggested group differences at a nominal p < 0.05. We used DAVID, a bioinformatics tool that provides functional interpretations of complex lists of genes, to examine representation of this gene list in known pathways. It confirmed that mechanisms related to immunity were the top significant associations with anhedonia in the sample. Further, the two top differentially expressed genes in our sample, IRF1 and GBP5, both have primary inflammation and immune functions, and were significantly negatively correlated with total scores on our self-report of anhedonia across all 48 subjects. These results suggest that prioritizing development of anti-inflammatory medications for CUD may pay dividends, particularly in combination with treatment-matching strategies using either phenotypic measures of anhedonia or biomarkers of inflammatory gene expression to individualize treatment. PUBMED: 30408130
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