technology with patient-derived iPS cell reprogramming techniques, may permit patient-derived organoids to aid as a bridge to shorten the glaring gap between disease modeling in the context of a human and animal models. However, the 3D organoids are devoid of their native microenvironment, which normally consists of stromal cells, muscle, blood vessels and immune cells (Dutta et al., 2017) and the human neurons in culture are probably still in early developmental stages, but certainly can be used for studying the impact of alcohol on this mini-brain structure, i.e. to model the pathophysiology of FASDs. Recent advancements utilizing the brain organoid to model human disorders or disease, from Zika viral (ZIKV) infection of human neurons (Qian, Nguyen, Jacob, Song, & Ming, 2017; Salick, Wells, Eggan, & Kaykas, 2017) to neuropsychiatric disorders (Quadrato, Brown, & Arlotta, 2016) to neurodegenerative disorders (Brawner, Xu, Liu, & Jiang, 2017), have yielded very important insights on human neuronal biology and pathophysiology. Nevertheless, modeling complex disorders like AUDs using neurocircuitry models holds the promise not only to provide great insights for understanding the underlying mechanism of AUDs but also provides a viable system for high throughput screening of effective drugs.
