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The Algorithmic Agent Perspective and Computational Neuropsychiatry: From Etiology to Advanced Therapy in Major Depressive Disorder

Giulio Ruffini, Francesca Castaldo, Edmundo Lopez-Sola, Roser Sanchez-Todo, Jakub Vohryzek

Entropy November 6, 2024 DOI: 10.3390/e26110953 via OpenAlex

Summary

AI-generated from the abstract

Major Depressive Disorder (MDD) is a complex condition that computational neuropsychiatry can help model mechanistically. Using the Kolmogorov theory of consciousness, a model was developed in which algorithmic agents interact with the world to maximize an Objective Function evaluating affective valence. Depression—defined as persistently low valence—may arise from inaccurate world models (cognitive biases), a dysfunctional Objective Function (anhedonia, anxiety), deficient planning (executive deficits), or unfavorable environments. The model maps to brain circuits and functional networks, linking with depression biotypes. Brain stimulation, psychotherapy, and psychedelics may synergistically repair neural circuits, with therapies optimized using personalized computational models.

Study at a glance

Characteristics Theoretical or philosophical paper Peer reviewed
Topics Depression
Keywords Neuropsychiatry Perspective graphical Etiology Psychotherapist
Citations 10
Key finding Depression can be modeled as a state of persistently low affective valence arising from factors including inaccurate world models, a dysfunctional Objective Function, deficient planning, or unfavorable environments.

Abstract

Major Depressive Disorder (MDD) is a complex, heterogeneous condition affecting millions worldwide. Computational neuropsychiatry offers potential breakthroughs through the mechanistic modeling of this disorder. Using the Kolmogorov theory (KT) of consciousness, we developed a foundational model where algorithmic agents interact with the world to maximize an Objective Function evaluating affective valence. Depression, defined in this context by a state of persistently low valence, may arise from various factors-including inaccurate world models (cognitive biases), a dysfunctional Objective Function (anhedonia, anxiety), deficient planning (executive deficits), or unfavorable environments. Integrating algorithmic, dynamical systems, and neurobiological concepts, we map the agent model to brain circuits and functional networks, framing potential etiological routes and linking with depression biotypes. Finally, we explore how brain stimulation, psychotherapy, and plasticity-enhancing compounds such as psychedelics can synergistically repair neural circuits and optimize therapies using personalized computational models.

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