Abstract
Objectives: Autism spectrum disorders (ASD) are characterized by qualitative impairment of social interactions, impairment of verbal and nonverbal communication, as well as restricted interests and repetitive behavior. ASD represent a group of complex psychiatric disorders, with both genetic and environmental factors implicated in their etiology. Recent neuroanatomical and epidemiological studies point out to prenatal and early postnatal genesis of ASD. Aim: In this review, we present recent studies that explored the effect of environmental, prenatal and perinatal risk factors on development of ASD. Also, we point out those factors that have been proven to have the strongest association with ASD, and emphasize a very complex interaction of individual factors that might eventually lead to manifestation of this group of disorders. Conclusion: A precise defining of risk factors might provide more insight not only into etiology of ASD, but might also give us a possibility for early recognition and possible prevention of autism spectrum disorders, especially in susceptible individuals. It is also a first step in defining the basis of the gene-environment interaction mechanism, which might enable the development of an individualized therapeutic approach for this group of disorders.
Highlights
The familial factorsThis group of factors include parental age and parity. through the replication process, leading to mutations [32]
Increased risk for Autism spectrum disorders (ASD) has been found in firstborns [34,35,36,37] the fourth and after the fourth child [35]
Neonatal risk factors for ASD are low birth weight, head circumference, low Apgar score, markers of hypoxia, respiratory distress syndrome, assisted ventilation, hyperbilirubinaemia, encephalopathy, congenital anomalies, and neonatal/congenital infections [28]. As it is shown in this review, different studies used different criteria for specific risk factors, and the results are mostly inconsistent
Summary
This group of factors include parental age and parity. through the replication process, leading to mutations [32]. A recent study of the whole genome sequencing including parents and offspring confirmed that about 80% of de novo mutations are paternal in origin, as well as that the number of mutations correlates with paternal age [33]
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