Alper Demirezen, Oytun Erbaş

Institute of Experimental Medicine, Gebze-Kocaeli, Türkiye

Keywords: Autism spectrum disorder, molecular biology, neurodevelopment, signaling pathway, transforming growth factor beta.


Autism spectrum disorder (ASD), a neurodevelopmental condition, is defined by challenges in social interaction and communication, repetitive behaviors, and focused or limited interests. The study of the molecular causes of ASD has advanced significantly in recent years. Transforming growth factor-beta (TGF-β) is a growth factor that is crucial for many biological processes, including synaptic plasticity, immune regulation, cell growth, and differentiation. According to research, the TGF-β signaling pathway abnormalities may be a factor in ASD. The influence of TGF-β on the regulation of the immune system, synaptic plasticity, and the development of the nervous system could potentially affect key aspects of ASD. It is well known that environmental, genetic, and epigenetic factors can all impact TGF-β activity. The TGF-β signaling pathway may offer therapeutic targets for ASD. The etiology and pathophysiology of ASD may benefit from potential therapeutic approaches that target TGF-β. In this review, we explained the definition and history of ASD, its relationship with its sociological impact, molecular biology, and the TGF-β signaling pathway, in addition to its symptoms and medical aspects.

Cite this article as: Demirezen A, Erbaş O. Autism spectrum disorder and the TGF-beta signalling pathway: Molecular relationships and therapeutic possibilities. D J Tx Sci 2023;8(1-2):1-26. doi: 10.5606/dsufnjt.2023.15.

Author Contributions

All authors contributed equally to the article.

Data Sharing Statement:
The data that support the findings of this study are available from the corresponding author upon reasonable request.

Conflict of Interest

The authors declared no conflicts of interest with respect to the authorship and/ or publication of this article.

Financial Disclosure

The authors received no financial support for the research and/or authorship of this article.