Consequences of trisomy 16 for mouse brain development: Corticogenesis in a model of Down syndrome

Tarik F. Haydar, Mary E. Blue, Mark E. Molliver, Bruce K. Krueger, Paul J. Yarowsky

Research output: Contribution to journalArticlepeer-review

Abstract

We have studied abnormalities in the tangential and radial expansion of the cerebral cortex during fetal development in the trisomy 16 (Ts16) mouse, a model for human trisomy 21 (Down syndrome). Slowed tangential expansion of the neuroepithelium in Ts16 resulted in a reduction of final telencephalic size and is predicted to decrease the number of radial cortical units in the mature brain. In addition, radial growth of the Ts16 cortex was delayed at the time of peak cortical neurogenesis in normal mice, but by embryonic day 18 the cortex reached normal thickness. Because mouse chromosome 16 shares many genes with human chromosome 21, abnormalities in Ts16 brain development may parallel abnormalities in trisomy 21.

Original languageEnglish (US)
Pages (from-to)6175-6182
Number of pages8
JournalJournal of Neuroscience
Volume16
Issue number19
DOIs
StatePublished - Oct 1 1996

Keywords

  • Down syndrome
  • cerebral cortex
  • development
  • histogenesis
  • mental retardation
  • trisomy 16

ASJC Scopus subject areas

  • Neuroscience(all)

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