Abstract
Reduced eye contact, facial expressions, and body movements during the first three years of life are among the social behaviors and nonverbal interactions that define autism spectrum disorder (ASD), a collection of neurodevelopmental diseases. It is generally accepted that this condition is a multifactorial disorder resulting from the combination of both hereditary and non-genetic risk factors. It is not a single disorder. Studies on the genetics of ASD have found mutations that disrupt normal neurodevelopment from infancy through childhood. Axon mobility and synaptogenesis have been linked to these gene complexes. Advances in neuroimaging research have yielded numerous significant insights into the pathological alterations that take place in the brains of individuals with ASD while they are living their lives. Numerous neuropathological and neuroimaging studies have demonstrated the significance of the amygdala, a key component of the limbic system and the affective loop of the cortico-striatothalamo-cortical circuit, in cognition and ASD. The nucleus accumbens is seen as another important structure associated with the social reward response in ASD, in addition to the amygdala. While behavioral and educational interventions have traditionally been the cornerstones of ASD care, pharmaceutical and interventional therapies have also demonstrated some promise in ASD patients. Additionally, a small number of individuals have reportedly improved following deep brain stimulation, one of the interventional treatments.
Published Version
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