**1. Introduction**

Communication between the gastrointestinal (GI) system and the central nervous system (CNS) occurs constantly and plays a critical role in maintaining the healthy status. That communication engages a bidirectional stimulation system, involving not only the brain and gut cells but endocrine-, immune-, and microbiota-derived components as well, the so-called gut-to-brain axis (GBA) [1, 2]. Consequently, impaired communication between both ends of the GBA, associated with or as consequence of disturbance of the GI microbial diversity, has been associated with a negative health outcome later in life [1, 3].

Increasing evidence points out that there is a link between alterations of gut microbiota and several disorders of the central nervous system including autism spectrum disorders (ASD) depression, anxiety, irritable bowel syndrome, attention deficit and hyperactivity disorder (ADHD), Parkinson's disease, disorders of mood and affect, and chronic pain [3–5].

The abovementioned psychiatric disorders frequently co-occur with each other, but interestingly they also occur in comorbidity with metabolic disorders, such as diabetes, cardiovascular disease, and metabolic syndrome [6–8], and are associated with adverse outcomes including higher mortality [6]. The insights of how those disorders are linked remain unclear. One likely explanation is that gut microbiota can trigger and guide the communication network of GBA and subsequently alter metabolic and psychological equilibrium [3, 5, 7, 8].

ASD are a heterogeneous set of lifelong neurodevelopmental diseases, whose incidence increased significantly over the past decades [9]. No unique etiology of ASD has been identified, though both genetic and environmental factors have been suggested [9, 10]. However, findings of candidate genes do not conclusively explain the etiopathology of ASD; thus, scientific research has been redirected to GI comorbidities of ASD, under the premise that the high frequency of gut microbiota alterations seen in these patients may be associated with autism symptoms severity [10]. Indeed, the independent observations of Rodakis [10] and Sandler et al. [11] about improvements in autism clinical manifestations after antibiotic treatments prompted intense research around the issue, including therapeutic interventions such as diet modification, supplementation with biotics (prebiotics, probiotics, synbiotics, and/or postbiotics), alternative antibiotic treatments, and fecal microbiota transplantation, among others, with variable outcomes [12].
