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تسجيل مستخدم جديدGenetic, Individual, and Familial Risk Correlates of Brain Network Controllability in Major Depressive Disorder
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Background: A therapeutic intervention in psychiatry can be viewed as an attempt to influence the brains large-scale, dynamic network state transitions underlying cognition and behavior. Building on connectome-based graph analysis and control theory, Network Control Theory is emerging as a powerful tool to quantify network controllability - i.e., the influence of one brain region over others regarding dynamic network state transitions. If and how network controllability is related to mental health remains elusive. Methods: From Diffusion Tensor Imaging data, we inferred structural connectivity and inferred calculated network controllability parameters to investigate their association with genetic and familial risk in patients diagnosed with major depressive disorder (MDD, n=692) and healthy controls (n=820). Results: First, we establish that controllability measures differ between healthy controls and MDD patients while not varying with current symptom severity or remission status. Second, we show that controllability in MDD patients is associated with polygenic scores for MDD and psychiatric cross-disorder risk. Finally, we provide evidence that controllability varies with familial risk of MDD and bipolar disorder as well as with body mass index. Conclusions: We show that network controllability is related to genetic, individual, and familial risk in MDD patients. We discuss how these insights into individual variation of network controllability may inform mechanistic models of treatment response prediction and personalized intervention-design in mental health.
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Mental disorders represent critical public health challenges as they are leading contributors to the global burden of disease and intensely influence social and financial welfare of individuals. The present comprehensive review concentrate on the two
mental disorders: Major depressive Disorder (MDD) and Bipolar Disorder (BD) with noteworthy publications during the last ten years. There is a big need nowadays for phenotypic characterization of psychiatric disorders with biomarkers. Electroencephalography (EEG) signals could offer a rich signature for MDD and BD and then they could improve understanding of pathophysiological mechanisms underling these mental disorders. In this review, we focus on the literature works adopting neural networks fed by EEG signals. Among those studies using EEG and neural networks, we have discussed a variety of EEG based protocols, biomarkers and public datasets for depression and bipolar disorder detection. We conclude with a discussion and valuable recommendations that will help to improve the reliability of developed models and for more accurate and more deterministic computational intelligence based systems in psychiatry. This review will prove to be a structured and valuable initial point for the researchers working on depression and bipolar disorders recognition by using EEG signals.
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ychopathology allowing us to formally derive a theoretical control energy which we hypothesize quantifies resistance to future symptom improvement in Major Depressive Disorder (MDD). We test this hypothesis and investigate the relation to genetic and environmental risk as well as resilience. Methods: We modelled longitudinal symptom-network dynamics derived from N=2,059 Beck Depression Inventory measurements acquired over a median of 134 days in a sample of N=109 patients suffering from MDD. We quantified the theoretical energy required for each patient and time-point to reach a symptom-free state given individual symptom-network topology (E 0 ) and 1) tested if E 0 predicts future symptom improvement and 2) whether this relationship is moderated by Polygenic Risk Scores (PRS) of mental disorders, childhood maltreatment experience, and self-reported resilience. Outcomes: We show that E 0 indeed predicts symptom reduction at the next measurement and reveal that this coupling between E 0 and future symptom change increases with higher genetic risk and childhood maltreatment while it decreases with resilience. Interpretation: Our study provides a mechanistic framework capable of predicting future symptom improvement based on individual symptom-network topology and clarifies the role of genetic and environmental risk as well as resilience. Our control-theoretic framework makes testable, quantitative predictions for individual therapeutic response and provides a starting-point for the theory-driven design of personalized interventions. Funding: German Research Foundation and Interdisciplinary Centre for Clinical Research, Munster
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