Abstract
Pre- and post-natal factors can affect brain development and function, impacting health outcomes with particular relevance to neurodevelopmental diseases, such as autism spectrum disorders (ASDs). Maternal obesity and its associated complications have been related to the increased risk of ASDs in offspring. Indeed, animals exposed to maternal obesity or high fat diets are prone to social communication impairment and repetitive behavior, the hallmarks of autism. During development, fatty acids and sugars, as well as satiety hormones, like insulin and leptin, and inflammatory factors related to obesity-induced low grade inflammation, could play a role in the impairment of neuroendocrine system and brain neuronal circuits regulating behavior in offspring. On the other side, post-natal factors, such as mode of delivery, stress, diet, or antibiotic treatment are associated to a modification of gut microbiota composition, perturbing microbiota-gut-brain axis. Indeed, the interplay between the gastrointestinal tract and the central nervous system not only occurs through neural, hormonal, and immune pathways, but also through microbe-derived metabolic products. The modification of unhealthy perinatal and postnatal environment, manipulation of gut microbiota, nutritional, and dietary interventions could represent possible strategies in preventing or limiting ASDs, through targeting inflammatory process and gut microbiota.
Highlights
Over the past decades, the frequency of autism diagnoses has been steadily climbing and has increased the interest of the scientific community (Fombonne, 2009; Boyle et al, 2011; Elsabbagh et al, 2012)
autism spectrum disorders (ASDs) is developed in children born prematurely (Limperopoulos et al, 2008; Abel et al, 2013; Moss and Chugani, 2014). These findings suggest that maternal obesity can raise the incidence of many negative elements, which in turn enhance the risk of developing ASD
Obesity results in an increased level of many inflammatory markers, as C reactive protein, IL- 6, IL-1β, and tumor necrosis factor (TNF)-α (Das, 2001). This relationship has been observed in pregnant obese women, leading to endothelial (Stewart et al, 2007), placental dysfunction (Leung and Bryant, 2000; Nordahl et al, 2008), and impaired fetal development contributing to the risk of ASD in children (Meyer et al, 2011)
Summary
The frequency of autism diagnoses has been steadily climbing and has increased the interest of the scientific community (Fombonne, 2009; Boyle et al, 2011; Elsabbagh et al, 2012). ASD is defined by impairments in social communication, repetitive behaviors, and restricted interests. Growing evidences suggest that individuals with ASDs present prominent activation of microglia and astrocytes and severe chronic inflammation (Vargas et al, 2005), both in the periphery and in multiple brain areas, characterized by increased levels of tumor necrosis factor (TNF)α (Al-Ayadhi, 2005; Chez et al, 2007), interleukin (IL)-1 (Al-Ayadhi, 2005), IL-6 (Wei et al, 2011), and interferon-γ (El-Ansary and Al-Ayadhi, 2012). It is noteworthy to better analyze the impact of all these factors on the behavior and physiology of future generations, thank to the support of the wide range of animal models resembling human pathophysiology of ASDs (Chadman, 2017) and whether efficacious intervention strategies can be optimized. Evidence associating ASDs to these different conditions will be better analyzed
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