Abstract
RETT syndrome is an X-chromosome-linked neurodevelopmental disorder mainly affecting female children, and its pathogenesis is mainly related to mutations in the Mecp2. In recent years, the role of Mecp2 in neurodevelopment and its relationship with RETT syndrome has become a hot research topic. Current research is focused on the effects of Mecp2 mutations on neuronal function and neural circuits, as well as exploring potential therapeutic approaches in animal models. Despite the results achieved, there are still gaps in the understanding of the precise molecular mechanisms of the Mecp2, gender specificity and the role of non-coding RNAs. This paper analyzed the role of Mecp2 in neurodevelopment and its relationship with Rett syndrome, and explored the molecular mechanisms and potential therapeutic strategies for Mecp2 mutations. It was found that Mecp2 mutations lead to neurological dysfunction by affecting neuronal differentiation and synaptic plasticity. In addition, this paper evaluates the current prospects for gene therapy, noting that adeno-associated viral vectors (AAV) have shown favorable therapeutic effects in animal experiments. This paper provides new insights into understanding the pathogenic mechanism of the Mecp2 in RETT syndrome and provides an important reference for future therapeutic strategies. However, the precise molecular mechanism of the Mecp2 and its gender-specific differences still need further investigation. Future studies could focus on developing safer and more effective gene therapies and exploring the role of non-coding RNAs in RETT syndrome with a view to achieving more comprehensive therapeutic strategies
Published Version
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