Abstract
Autism spectrum disorders (ASD) are a group of early-onset neurodevelopmental conditions characterized by alterations in brain connectivity with cascading effects on neuropsychological functions. To date, in the framework of an increasing interest about environmental conditions which could interact with genetic factors in ASD pathogenesis, many authors have stressed that changes in the intrauterine environment at different stages of pregnancy, such as those linked to maternal metabolic pathologies, may lead to long-term conditions in the newborn. In particular, a growing number of epidemiological studies have highlighted the role of obesity and maternal diabetes as a risk factor for developing both somatic and psychiatric disorders in humans, including ASD. While literature still fails in identifying specific etiopathological mechanisms, a growing body of evidence is available about the presence of a relationship between maternal immune dysregulation, inflammation, oxidative stress, and the development of ASD in the offspring. In this framework, results from high-fat diet animal models about the role played by oxidative stress in shaping offspring neurodevelopment may help in clarifying the pathways through which maternal metabolic conditions are linked with ASD. The aim of this review is to provide an overview of literature about the effects of early life insults linked to oxidative stress which may be involved in ASD etiopathogenesis and how this relationship can be explained in biological terms.
Highlights
Brain development in a fetus and in the first years of life is pivotal in the shaping of the individual overall neuropsychological performance level [1,2,3]
The aim of this paper is to review evidence from literature, regarding whether the effects of early life insults and that linked to oxidative stress in particular might be involved in short- and long-term risks for autism spectrum disorder (ASD) and how this risk can be explained in biological terms
In the framework of a growing interest about possible environmental factors involved in the etiopathogenesis of ASD, in particular during in utero life, increasing epidemiological reports highlighted the link between ASD and maternal metabolic conditions
Summary
Brain development in a fetus and in the first years of life is pivotal in the shaping of the individual overall neuropsychological performance level [1,2,3]. The Sasaki et al [57] rat model showed how high-fat diet consumption during pregnancy and lactation led to an offspring with decreased basal corticosterone levels but heightened response to stress with a slower restoration of baseline corticosterone This offspring showed an increase in glucocorticoid receptors in the amygdala, with a concurrent alteration in inflammatory gene expression for the hippocampus and amygdala. A nonhuman primate model showed that maternal high-fat diet consumption impaired the development of the serotonergic system, leading to a reduction of serotonin synthesis and increased anxiety behaviors in the female offspring [33] This model shows increased inflammation levels in the hypothalamus among mothers and offspring [33, 44]. Another study stressed the involvement of genetic expression in this process, showing in a rat that maternal high-fat dietinduced obesity led to dopamine dysregulation in the offspring by the means of genome-wide methylation and gene regulation for dopamine reuptake trasporter, the μ-opioid receptor and preproenkephalin [60]
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