Correlations between neuroendocrine disorders and biochemical brain metabolites alterations in antidepressant treatment

Abstract

We approach the theme of modern investigation and treatment strategies, based on biochemical, clinicalbiological, metabolic, pharmacogenetic, neuro-imagistic, and neuroendocrine integrative correlations in the management of depressive disorders. Our main objective was to investigate: The biochemical brain metabolites [N-Acetyl-Aspartate (NAA), gamma-Aminobutyric acid (GABA), aspartate (Asp), creatine (CR), glutamine (Gln), glicerophosphocholine (GPC), phosphocholine (PC), phosphocreatine (PCR), taurine (Tau), N-methyl-D-Aspartate (N-MDA), serine, glycine, choline (Cho)]; the neuroimagistic and neurobiological markers and the metabolic abnormalities in correlation with the molecular pharmacogenetic testing in children and adolescents treated with antidepressant medication. Our research was conducted between 2009-2016 on 90 children and adolescents with depressive disorders -45 children-G1, who benefited of pharmacogenetic testing tailored pharmacotherapy, and 45 without pharmacogenetic testing-G2. The patients were also evaluated by MR spectroscopy at baseline and after pharmacotherapy. The efficacy of the chosen therapy in correlation with the pharmacogenetic testing was evaluated by the mean change in the CDRS (Child Depression Rating Scale) total scores, in the CGI-S/I (Clinical Global Impression Severity/ Improvement), CGAS (Clinical Global Assessment of Functioning) and by the change of the relevant neurobiological markers and MR spectroscopy biochemical brain metabolites. Our results showed statistically significant differences in the clinical scores between the studied groups. Our research could represent a proof that the biochemical brain metabolites registered in depressive disorders modified values in the MR spectroscopy and the administration of antidepressants could determine metabolic and neuroendocrine abnormalities (changed lipid profiles, high insulin and plasma glucose levels, weight gain, obesity), especially when chosen without prior pharmacogenetic testing.