This paper introduces a higher-order adaptive self-modelling network model to simulate the role of epigenetics in the development and treatment of Rett syndrome (RTT). RTT is a neurodevelopmental disorder caused by mutations in the MECP2 gene. The model is constructed using temporal-causal network modeling principles and integrates multiple levels of biological and emotional adaptation. While MECP2 dysfunction is central to RTT, recent findings emphasize the role of environmental factors, mainly early-life stress. One of the epigenetic consequences of this stress, is the reduced expression of brain-derived neurotrophic factor (BDNF) and widespread dysfunction in emotional and cognitive regulation. In this study, a computational simulation is used to explore both the development of RTT and the potential effectiveness of a hypothetical epigenetic therapy aimed at restoring BDNF expression. The results highlight how targeted intervention could reverse or mitigate the long-term neurological impacts of RTT.

错误:搜索内容不能为空,请输入英文关键词
错误:关键词超出字数限制,请精简
高级检索

Higher-Order Adaptive Dynamical System Modeling of the Role of Epigenetics in Rett Syndrome

  • Marwa Tinmiouli,
  • Sophie C. F. Hendrikse,
  • Jan Treur

摘要

This paper introduces a higher-order adaptive self-modelling network model to simulate the role of epigenetics in the development and treatment of Rett syndrome (RTT). RTT is a neurodevelopmental disorder caused by mutations in the MECP2 gene. The model is constructed using temporal-causal network modeling principles and integrates multiple levels of biological and emotional adaptation. While MECP2 dysfunction is central to RTT, recent findings emphasize the role of environmental factors, mainly early-life stress. One of the epigenetic consequences of this stress, is the reduced expression of brain-derived neurotrophic factor (BDNF) and widespread dysfunction in emotional and cognitive regulation. In this study, a computational simulation is used to explore both the development of RTT and the potential effectiveness of a hypothetical epigenetic therapy aimed at restoring BDNF expression. The results highlight how targeted intervention could reverse or mitigate the long-term neurological impacts of RTT.