OSVZ progenitors in the human cortex: an updated perspective on neurodevelopmental disease. LaMonica, B. E, Lui, J. H, Wang, X., & Kriegstein, A. R Curr Opin Neurobiol, 22(5):747–753, April, 2012.
abstract   bibtex   
Recent discoveries concerning the architecture and cellular dynamics of the developing human brain are revealing new differences between mouse and human cortical development. In mice, neurons are produced by ventricular radial glial (RG) cells and subventricular zone intermediate progenitor (IP) cells. In the human cortex, both ventricular RG and highly motile outer RG cells generate IP cells, which undergo multiple rounds of transit amplification in the outer subventricular zone before producing neurons. This creates a more complex environment for neurogenesis and neuronal migration, adding new arenas in which neurodevelopmental disease gene mutation could disrupt corticogenesis. A more complete understanding of disease mechanisms will involve use of emerging model systems with developmental programs more similar to that of the human neocortex.
@ARTICLE{LaMonica2012-py,
  title    = "{OSVZ} progenitors in the human cortex: an updated perspective on
              neurodevelopmental disease",
  author   = "LaMonica, Bridget E and Lui, Jan H and Wang, Xiaoqun and
              Kriegstein, Arnold R",
  abstract = "Recent discoveries concerning the architecture and cellular
              dynamics of the developing human brain are revealing new
              differences between mouse and human cortical development. In
              mice, neurons are produced by ventricular radial glial (RG) cells
              and subventricular zone intermediate progenitor (IP) cells. In
              the human cortex, both ventricular RG and highly motile outer RG
              cells generate IP cells, which undergo multiple rounds of transit
              amplification in the outer subventricular zone before producing
              neurons. This creates a more complex environment for neurogenesis
              and neuronal migration, adding new arenas in which
              neurodevelopmental disease gene mutation could disrupt
              corticogenesis. A more complete understanding of disease
              mechanisms will involve use of emerging model systems with
              developmental programs more similar to that of the human
              neocortex.",
  journal  = "Curr Opin Neurobiol",
  volume   =  22,
  number   =  5,
  pages    = "747--753",
  month    =  apr,
  year     =  2012,
  language = "en"
}

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