Neuroinflammation and autism: what have we learned so far?

Abstract

The purpose of the review is to summarize clinical and preclinical study data from the literature related to the relationship between autism and inflammation, as well as hypotheses associated with this relationship. Autism is a neurodevelopmental disorder with an increasing prevalence, yet limited data regarding its etiology. Inflammatory changes are thought to potentially play a role in the pathogenesis of autism. It has been demonstrated that the frequency of autoimmune diseases is higher in the families of individuals with autism, and there is an increased risk of autoimmune diseases in these individuals. Some immune system-related molecules such as cytokines and chemokines have also been shown to play a role in the etiology of autism, affecting synapse development, plasticity, and consequently, the development of cortical connections. Preclinical and clinical studies are being conducted on the use of exosomes, small lipid-surfaced vesicles capable of crossing the blood–brain barrier, to regulate inflammation-associated molecules and signaling pathways shown to exhibit differences in individuals with autism. Additionally, research is ongoing regarding the modulation of the mTOR pathway, probiotics which have gained attention for correcting dysbiosis, and drugs like luteolin and minocycline, known to inhibit microglial activation. However, the evidence supporting their effectiveness remains limited. While the literature contains a wealth of data regarding the relationship between autism and inflammation, it is important to acknowledge that many findings remain contradictory. Nevertheless, the exploration of neuroinflammation and its associated treatments provides a promising avenue for furthering our understanding of autism spectrum disorder.

Keywords:

• Autism
• inflammation
• antibody
• cytokine
• exosome

Acknowledgments

The authors of this work do not wish to make any special acknowledgments.

Authors’ contributions

A.A. Synthesized information from diverse sources and drafted the manuscript. D.Ü. Supervised the overall review process, offering guidance on content, structure, and coherence.

Disclosure statement

No potential conflict of interest was reported by the authors.

Data availability statement

We confirm that this review article does not contain any original data as it is a synthesis of existing literature. All information and findings presented in this review are based on publicly available sources and previously published research articles, which are appropriately cited within the text. No additional data were generated for this review.