GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE19nnn/GSE19738/primaryOK2000000GenomicsHomo sapiensExpression profiling by arrayhttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE19738GEOGSE0falseMajor Depressive Disorder blood gene expressionBackground: Major Depressive Disorder (MDD) is a moderately heritable disorder with a high lifetime prevalence. At present, laboratory blood tests to support MDD diagnosis are not available. Methods: We used a classifier approach on blood gene expression profiles of a unique set of non-medicated subjects (MDD patients and controls) to select genes of which expression is predictive for disease status. To reveal blood gene expression changes related to MDD disease, we applied a powerful ex vivo stimulus to the blood, i.e. incubation with lipopolysaccharide (LPS; 10 ng/ml blood). Results: Based on LPS-stimulated blood gene expression using whole-genome microarrays in 42 subjects (primary cohort; 21 MDD patients (mean age 42.3 years), 21 healthy controls (mean age 41.9 years)), we identified a set of genes (CAPRIN1, CLEC4A, KRT23, MLC1, PLSCR1, PROK2, ZBTB16) that serves as a molecular signature of MDD. These findings were validated for the primary cohort using an independent quantitative PCR method (P = 0.007). The difference between depressive patients and controls was confirmed (P = 0.019) in a replication cohort of 13 patients with MDD (mean age 42.8 years) and 14 controls (mean age 45.6 years). The MDD-signature score comprised of expression levels of 7 genes could discriminate depressive patients from controls with sensitivity of 76.9% and specificity of 71.8%. Conclusions: We show for the first time that molecular analysis of stimulated blood cells can be used as an endophenotype for MDD diagnosis, which is a milestone in establishing biomarkers for neuropsychiatric disorders with moderate heritability in general. Our results may provide a new entry point for following and predicting treatment outcome, as well as prediction of severity and recurrence of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 sapiens[20471630]