Laura Kranaster1, Carolin Hoyer2, Suna S Aksay3, J Malte Bumb4, Norbert Müller5,6, Peter Zill5, Markus J Schwarz7, Natalie Moll7, Beat Lutz8, Laura Bindila8, Inga Zerr9, Matthias Schmitz9, Kaj Blennow10,11, Henrik Zetterberg10,11,12,13, Dieter Haffner14, Maren Leifheit-Nestler14, Cagakan Ozbalci15,16, Christoph Janke17, Manfred Thiel17, Alexander Sartorius3. 1. Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim/Heidelberg University, Mannheim, Germanylaura.kranaster@zi-mannheim.de. 2. Department of Neurology, University Medical Centre Mannheim, Mannheim, Germany. 3. Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim/Heidelberg University, Mannheim, Germany. 4. Department of Addictive Behavior and Addiction Medicine, Central Institute of Mental Health, Medical Faculty Mannheim/Heidelberg University, Mannheim, Germany. 5. Department of Psychiatry and Psychotherapy, Ludwig Maximilian University Munich, Munich, Germany. 6. Marion von Tessin Memory-Zentrum, Munich, Germany. 7. Institute of Laboratory Medicine, University Hospital LMU Munich, Munich, Germany. 8. Institute for Physiological Chemistry, University Medical Center Mainz of the Johannes Gutenberg University Mainz, Mainz, Germany. 9. Department of Neurology, University Medical Center Göttingen and the German Center for Neurodegenerative Diseases (DZNE), Göttingen, Germany. 10. Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden. 11. Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden. 12. Department of Molecular Neuroscience, UCL Institute of Neurology, London, United Kingdom. 13. UK Dementia Research Institute at UCL, London, United Kingdom. 14. Department of Pediatric Kidney, Liver and Metabolic Diseases, Hannover Medical School, Hannover, Germany. 15. Randall Centre for Cell and Molecular Biophysics, King's College London, London, United Kingdom. 16. Heidelberg University Biochemistry Center, Heidelberg, Germany. 17. Department of Anesthesiology and Critical Care Medicine, University Medical Centre Mannheim, Mannheim, Germany.
Abstract
BACKGROUND: No candidate biomarkers based on cerebrospinal fluid (CSF) have been identified as prognostic factors in patients with major depression treated with electroconvulsive therapy (ECT), yet. METHOD: Following different underlying hypotheses, we analysed baseline CSF levels of markers of neurodegeneration (tau proteins, β-amyloids and neurogranin), elements of the innate immune system (interleukin [IL]-6, neopterin, soluble CD14, soluble CD163, migration inhibitory factor and monocyte chemotactic protein 1), endocannabinoids, sphingolipids and Klotho before ECT in patients with depression (n = 12) to identify possible correlations with the clinical antidepressant response to ECT. RESULTS: Correlation with the reduction of the depressive symptoms could be observed especially for markers of neurodegeneration and elements of the innate immune system. Differences for CSF levels of several markers were found between the groups of responders and non-responders at the trend level. LIMITATIONS: The sample size is small and the -distribution of responders and non-responders is uneven. CONCLUSIONS: It is this first study on CSF biomarkers for antidepressant efficacy of ECT warrants further research regarding the mechanism of ECT and personalized antidepressant therapy.
BACKGROUND: No candidate biomarkers based on cerebrospinal fluid (CSF) have been identified as prognostic factors in patients with major depression treated with electroconvulsive therapy (ECT), yet. METHOD: Following different underlying hypotheses, we analysed baseline CSF levels of markers of neurodegeneration (tau proteins, β-amyloids and neurogranin), elements of the innate immune system (interleukin [IL]-6, neopterin, soluble CD14, soluble CD163, migration inhibitory factor and monocyte chemotactic protein 1), endocannabinoids, sphingolipids and Klotho before ECT in patients with depression (n = 12) to identify possible correlations with the clinical antidepressant response to ECT. RESULTS: Correlation with the reduction of the depressive symptoms could be observed especially for markers of neurodegeneration and elements of the innate immune system. Differences for CSF levels of several markers were found between the groups of responders and non-responders at the trend level. LIMITATIONS: The sample size is small and the -distribution of responders and non-responders is uneven. CONCLUSIONS: It is this first study on CSF biomarkers for antidepressant efficacy of ECT warrants further research regarding the mechanism of ECT and personalized antidepressant therapy.