Modeling human neuronal migration deficits in 3D

During the past few decades, we have witnessed an impressive gain in the knowledge regarding the basic mechanisms underlying human neuronal migration disorders by the usage of mouse models. Nevertheless, despite the remarkable conservation both in the genetic encoded information and the developmental processes, there are still numerous important differences between human and mouse. This may explain the vast excitement following the realization that technological breakthroughs enabled generating tissue-like human-based organoids for modeling human neuronal migration diseases. This review will provide a short introduction on human and mouse neuronal migration processes, and highlight human brain organoid models of neuronal migration diseases. Schematic presentation of migratory routes in the developing mouse and human brain. (a) In mouse and human fetal brain there are at least three sites of origin of the Cajal Retzius (CR) cells; namely (1) the cortical hem (CH), (2) the septum (SP) and (3) the pallial subpallial boundary (PSB). CR cells derived from all these three regions differ in gene expression, morphology and the undertaken migratory route. Despite certain similarities the kinetics and timeline of migration differ between human and rodents. (b) Both in human and rodent brains, new-born neurons exhibit radial

Automated summary

Advancements in understanding human neuronal migration disorders using mouse models have been significant, despite the notable differences between human and mouse genetic information and developmental processes. The development of human brain organoid models has sparked excitement in modeling human neuronal migration diseases. Differences in gene expression, morphology, and migratory routes between human and mouse brains highlight the need for further study.