Divyangana Rakesh1, Clare Kelly2, Nandita Vijayakumar3, Andrew Zalesky4, Nicholas B Allen5, Sarah Whittle6. 1. Melbourne Neuropsychiatry Centre, Department of Psychiatry, University of Melbourne and Melbourne Health, Carlton, Australia. Electronic address: divyangana.rakesh@gmail.com. 2. Trinity College Institute of Neuroscience, Trinity College Dublin, Dublin, Ireland. 3. School of Psychology, Deakin University, Melbourne, Australia. 4. Melbourne Neuropsychiatry Centre, Department of Psychiatry, University of Melbourne and Melbourne Health, Carlton, Australia; Melbourne School of Engineering, University of Melbourne, Melbourne, Victoria, Australia. 5. Department of Psychology, University of Oregon, Eugene, Oregon. 6. Melbourne Neuropsychiatry Centre, Department of Psychiatry, University of Melbourne and Melbourne Health, Carlton, Australia. Electronic address: swhittle@unimelb.edu.au.
Abstract
BACKGROUND: Childhood maltreatment is associated with lifelong psychiatric sequelae. However, our understanding of neurobiological mechanisms responsible for this association is limited. Childhood maltreatment may confer risk for psychopathology by altering neurodevelopmental trajectories during childhood and adolescence. Longitudinal research, which is essential for examining this question, has been limited. METHODS: We investigated maltreatment-associated alterations in the development of neural circuitry. Associations between cumulative childhood maltreatment (assessed using a dimensional measure of abuse and neglect via the Childhood Trauma Questionnaire) and the longitudinal development of resting-state functional connectivity (rsFC) were examined in 130 community-residing adolescents. Functional magnetic resonance imaging data were acquired at age 16 (T1; mean ± SD age, 16.46 ± 0.52 years; 66 females) and age 19 (T2; mean follow-up period, 2.35 years; n = 90 with functional magnetic resonance imaging data at both time points). RESULTS: We found maltreatment to be associated with widespread longitudinal increases in rsFC, primarily between default mode, dorsal attention, and frontoparietal systems. We also found sex-dependent increased maltreatment-associated rsFC in male participants in salience and limbic circuits. Cross-sectional analyses revealed a shift in maltreatment-related rsFC alterations, which were localized to subcortical and sensory circuits at T1 and to frontal circuits at T2. Finally, longitudinal increases in rsFC connectivity mediated the relationship between childhood maltreatment and increased depressive symptoms. CONCLUSIONS: To our knowledge, this is the first study to examine longitudinal maltreatment-related alterations in rsFC in adolescents. Our findings shed light on the neurodevelopmental consequences of childhood maltreatment and provide evidence for their role in risk for depression.
BACKGROUND: Childhood maltreatment is associated with lifelong psychiatric sequelae. However, our understanding of neurobiological mechanisms responsible for this association is limited. Childhood maltreatment may confer risk for psychopathology by altering neurodevelopmental trajectories during childhood and adolescence. Longitudinal research, which is essential for examining this question, has been limited. METHODS: We investigated maltreatment-associated alterations in the development of neural circuitry. Associations between cumulative childhood maltreatment (assessed using a dimensional measure of abuse and neglect via the Childhood Trauma Questionnaire) and the longitudinal development of resting-state functional connectivity (rsFC) were examined in 130 community-residing adolescents. Functional magnetic resonance imaging data were acquired at age 16 (T1; mean ± SD age, 16.46 ± 0.52 years; 66 females) and age 19 (T2; mean follow-up period, 2.35 years; n = 90 with functional magnetic resonance imaging data at both time points). RESULTS: We found maltreatment to be associated with widespread longitudinal increases in rsFC, primarily between default mode, dorsal attention, and frontoparietal systems. We also found sex-dependent increased maltreatment-associated rsFC in male participants in salience and limbic circuits. Cross-sectional analyses revealed a shift in maltreatment-related rsFC alterations, which were localized to subcortical and sensory circuits at T1 and to frontal circuits at T2. Finally, longitudinal increases in rsFC connectivity mediated the relationship between childhood maltreatment and increased depressive symptoms. CONCLUSIONS: To our knowledge, this is the first study to examine longitudinal maltreatment-related alterations in rsFC in adolescents. Our findings shed light on the neurodevelopmental consequences of childhood maltreatment and provide evidence for their role in risk for depression.
Authors: Layla Banihashemi; Christine W Peng; Anusha Rangarajan; Helmet T Karim; Meredith L Wallace; Brandon M Sibbach; Jaspreet Singh; Mark M Stinley; Anne Germain; Howard J Aizenstein Journal: Front Psychol Date: 2022-03-03