Arne Doose1, Inger Hellerhoff2, Friederike I Tam2, Joseph A King1, Maria Seidel1, Daniel Geisler1, Hans Christian I Plähn1, Veit Roessner3, Katja Akgün4, Tjalf Ziemssen4, Stefan Ehrlich5. 1. Translational Developmental Neuroscience Section, Division of Psychological and Social Medicine and Developmental Neuroscience, Faculty of Medicine, Technische Universität Dresden, Dresden, Germany. 2. Translational Developmental Neuroscience Section, Division of Psychological and Social Medicine and Developmental Neuroscience, Faculty of Medicine, Technische Universität Dresden, Dresden, Germany; Eating Disorder Research and Treatment Center, Department of Child and Adolescent Psychiatry, Faculty of Medicine, Technische Universität Dresden, Dresden, Germany. 3. Department of Child and Adolescent Psychiatry, Faculty of Medicine, University Hospital Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany. 4. Center of Clinical Neuroscience, Neurological Clinic, University Hospital Carl Gustav Carus, Faculty of Medicine, Technische Universität Dresden, Dresden, Germany. 5. Translational Developmental Neuroscience Section, Division of Psychological and Social Medicine and Developmental Neuroscience, Faculty of Medicine, Technische Universität Dresden, Dresden, Germany; Eating Disorder Research and Treatment Center, Department of Child and Adolescent Psychiatry, Faculty of Medicine, Technische Universität Dresden, Dresden, Germany. Electronic address: transden.lab@uniklinikum-dresden.de.
Abstract
PURPOSE: The acute state of anorexia nervosa (AN) is accompanied by increased peripheral concentrations of brain-derived damage markers indicative of ongoing neural and glial damage processes. Although these findings correspond with well-documented structural brain changes in the disorder, it remains unclear whether abnormal levels of brain-derived damage markers persist after long-term weight-recovery from AN. METHODS: To address this question, we used single-molecule array (Simoa) technology to measure serum levels of neurofilament light (NF-L), tau protein and glial fibrillary acidic protein (GFAP) in a group of 55 long-term weight-recovered women with a history of AN (recAN) and 55 age-matched healthy controls. Strict exclusion criteria allowed us to control for confounds present in previous studies including most importantly neurological conditions. RESULTS: We found not only no group differences but also statistical evidence for equal damage marker levels between groups using Bayesian hypothesis testing. CONCLUSION: These results provide evidence for the absence of neuronal and glial damage processes after long-term weight-recovery from AN. Together, our findings are indicative of complete normalization following long-term weight restoration provide hope that recovery from AN halts neuronal damage processes and support the need to test potential candidates for therapeutic interventions including pharmacological neuroprotection.
PURPOSE: The acute state of anorexia nervosa (AN) is accompanied by increased peripheral concentrations of brain-derived damage markers indicative of ongoing neural and glial damage processes. Although these findings correspond with well-documented structural brain changes in the disorder, it remains unclear whether abnormal levels of brain-derived damage markers persist after long-term weight-recovery from AN. METHODS: To address this question, we used single-molecule array (Simoa) technology to measure serum levels of neurofilament light (NF-L), tau protein and glial fibrillary acidic protein (GFAP) in a group of 55 long-term weight-recovered women with a history of AN (recAN) and 55 age-matched healthy controls. Strict exclusion criteria allowed us to control for confounds present in previous studies including most importantly neurological conditions. RESULTS: We found not only no group differences but also statistical evidence for equal damage marker levels between groups using Bayesian hypothesis testing. CONCLUSION: These results provide evidence for the absence of neuronal and glial damage processes after long-term weight-recovery from AN. Together, our findings are indicative of complete normalization following long-term weight restoration provide hope that recovery from AN halts neuronal damage processes and support the need to test potential candidates for therapeutic interventions including pharmacological neuroprotection.