Neuroinflammation and autism: what have we learned so far?

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.