Autism spectrum disorder (ASD) remains a public health concern, as recent prevalence estimates of ASD are as high as 1 in 44 (Maenner et al., 2021). Despite the burden imposed by ASD, limited progress has been achieved in unraveling etiologies, biological mechanisms, or pharmacological intervention (Lord et al., 2020). While research provides valuable input (Bhandari, Paliwal, & Kuhad, 2020), the translation of results from bench to bedside remains slow and ineffective. This shortcoming led to a plethora of models seeking to provide insight into how ASD arises, spanning from genetics to cognitive theories (Lord et al., 2020). One of these models is what we designated “the dopamine hypothesis of ASD” (Pavăl and Micluția, 2021, Pavăl, 2017).

In this chapter, we aim to provide a comprehensive picture of the dopaminergic model we previously proposed. To achieve this, we will start by summarizing the previous versions of our hypothesis. Afterwards, we will review in detail the studies that provide empirical evidence and support for our model. Last, we will debate future prospects with an emphasis on newly-developed methods of testing our hypothesis.