A biomarker to differentiate between primary and cocaine-induced major depression in cocaine use disorder: the role of platelet IRAS/Nischarin (I1-Imidazoline Receptor)

Keller, Benjamin; Mestre-Pintó, Juan Ignacio; Álvaro-Bartolomé, María; Martínez-Sanvisens, Diana; Farré Albaladejo, Magí; García-Fuster, M. Julia; García Sevilla, Jesús; Torrens, Marta; The NEURODEP Group

doi:http://dx.doi.org/10.3389/fpsyt.2017.00258

A biomarker to differentiate between primary and cocaine-induced major depression in cocaine use disorder: the role of platelet IRAS/Nischarin (I1-Imidazoline Receptor)

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Keller B, Mestre-Pinto JI, Álvaro-Bartolomé M, Martinez-Sanvisens D, Farre M, García-Fuster MJ. Et al. A biomarker to differentiate between primary and cocaine-induced major depression in cocaine use disorder: the role of platelet IRAS/Nischarin (I1-Imidazoline Receptor). Front Psychiatry. 2017 Dec 1;8:258. DOI: 10.3389/fpsyt.2017.00258

Abstract

The association of cocaine use disorder (CUD) and comorbid major depressive disorder (MDD; CUD/MDD) is characterized by high prevalence and poor treatment outcomes. CUD/MDD may be primary (primary MDD) or cocaine-induced (CUD-induced MDD). Specific biomarkers are needed to improve diagnoses and therapeutic approaches in this dual pathology. Platelet biomarkers [5-HT2A receptor and imidazoline receptor antisera selected (IRAS)/nischarin] were assessed by Western blot in subjects with CUD and primary MDD (n = 16) or CUD-induced MDD (n = 9; antidepressant free, AD-; antidepressant treated, AD+) and controls (n = 10) at basal level and/or after acute tryptophan depletion (ATD). Basal platelet 5-HT2A receptor (monomer) was reduced in comorbid CUD/MDD subjects (all patients: 43%) compared to healthy controls, and this down-regulation was independent of AD medication (decreases in AD-: 47%, and in AD+: 40%). No basal differences were found for IRAS/nischarin contents in AD+ and AD- comorbid CUD/MDD subjects. The comparison of IRAS/nischarin in the different subject groups during/after ATD showed opposite modulations (i.e., increases and decreases) in response to low plasma tryptophan levels with significant differences discriminating between the subgroups of CUD with primary MDD and CUD-induced MDD. These specific alterations suggested that platelet IRAS/nischarin might be useful as a biomarker to discriminate between primary and CUD-induced MDD in this dual pathology.