One very recent example of modeling neurodevelopmental disorders primarily driven by environmental factors is the modeling of Zika infection with brain organoids. Modeling infection in early embryonic stages, as would be the case when modeling with hiPSCs, can be useful in predicting some problems later on in life. hiPSCs have allowed these researchers to investigate areas of the disease’ biology that were previously intractable – such as what the Zika virus actually targets in embryonic stages that results in the various physical birth anomalies (e.g., microecephaly) and later issues in brain development. In the small period of time since when Zika became a critical public health concern, researchers have been able to isolate exactly why babies born from Zika virus infected mothers had microcephaly. Tang et al. showed that the virus readily infects forebrain-specific cortical neural progenitors, the building blocks of the human cortex 166. The same study went further to show that at the molecular level the infection resulted in downregulation of cell-cycle genes and upregulation of apoptosis genes in NPCs. This was further evidenced by abnormal progression of
