Thibaut Gelle1, Rayhanatou Altine Samey1, Brigitte Plansont2, Barbara Bessette3, Marie-Odile Jauberteau-Marchan3, Fabrice Lalloué3, Murielle Girard4. 1. Unité de Recherche et de Neurostimulation, Centre Hospitalier Esquirol, 15 rue du Docteur Marcland, 87025 Limoges Cedex, France; INSERM, UMR 1094, Neuroépidémiologie Tropicale, Faculté de Médecine, Université de Limoges, 2 avenue Martin Luther King, Limoges, France. 2. Unité de Recherche et de Neurostimulation, Centre Hospitalier Esquirol, 15 rue du Docteur Marcland, 87025 Limoges Cedex, France. 3. EA 3842 Homéostasie Cellulaire et Pathologies, Faculté de Médecine, Université de Limoges, 2 avenue Martin Luther King, Limoges, France. 4. Unité de Recherche et de Neurostimulation, Centre Hospitalier Esquirol, 15 rue du Docteur Marcland, 87025 Limoges Cedex, France; INSERM, UMR 1094, Neuroépidémiologie Tropicale, Faculté de Médecine, Université de Limoges, 2 avenue Martin Luther King, Limoges, France. Electronic address: Murielle.girard@ch-esquirol-limoges.fr.
Abstract
BACKGROUND: The study of clinically related biological indicators in Major Depression (MD) is important. The Brain Derived Neurotrophic Factor (BDNF) appears to play an important role in MD, through its neurotrophic effect, and its levels are significantly decreased. The variation in the serum levels of its precursor proBDNF, which has opposite effects, is not known. Their distribution between serum and exosomes and their evolution during antidepressant treatment is also not known, and may be important in modulating their effects. The aim of this study is to evaluate whether serum and exosome mBDNF and proBDNF levels are altered in patients with MD during antidepressant treatment compared to controls, and their association with clinical improvement and clinical variables. MATERIALS AND METHODS: 42 MD subjects and 40 controls were included. Questionnaires to assess the severity of depression and cognitive impairment and blood samples were collected during the three visits at D0 (inclusion) and 3 and 7 weeks after the start of antidepressant treatment. Assays for mBDNF and proBDNF levels were performed in serum and exosomes by ELISA. RESULTS: MD subjects had decreased serum and exosomal BDNF levels and increased proBDNF levels at D0 compared to controls. BDNF and pro-BDNF vary in an inverse manner in both serum and exosomes during antidepressant treatment. No relationship of BDNF and proBDNF levels to clinical improvement and depression scales was found. CONCLUSION: We demonstrated an evolution of those molecules either in serum or in exosomes after MD treatment. These transport vesicles could have a role in the regulation of BDNF.
BACKGROUND: The study of clinically related biological indicators in Major Depression (MD) is important. The Brain Derived Neurotrophic Factor (BDNF) appears to play an important role in MD, through its neurotrophic effect, and its levels are significantly decreased. The variation in the serum levels of its precursor proBDNF, which has opposite effects, is not known. Their distribution between serum and exosomes and their evolution during antidepressant treatment is also not known, and may be important in modulating their effects. The aim of this study is to evaluate whether serum and exosome mBDNF and proBDNF levels are altered in patients with MD during antidepressant treatment compared to controls, and their association with clinical improvement and clinical variables. MATERIALS AND METHODS: 42 MD subjects and 40 controls were included. Questionnaires to assess the severity of depression and cognitive impairment and blood samples were collected during the three visits at D0 (inclusion) and 3 and 7 weeks after the start of antidepressant treatment. Assays for mBDNF and proBDNF levels were performed in serum and exosomes by ELISA. RESULTS: MD subjects had decreased serum and exosomal BDNF levels and increased proBDNF levels at D0 compared to controls. BDNF and pro-BDNF vary in an inverse manner in both serum and exosomes during antidepressant treatment. No relationship of BDNF and proBDNF levels to clinical improvement and depression scales was found. CONCLUSION: We demonstrated an evolution of those molecules either in serum or in exosomes after MD treatment. These transport vesicles could have a role in the regulation of BDNF.
Authors: Stephen Breazeale; Samantha Conley; Sangchoon Jeon; Susan G Dorsey; Joan Kearney; Brad Yoo; Nancy S Redeker Journal: Injury Date: 2022-03-22 Impact factor: 2.687