Differential gene expression studies to explore the molecular pathophysiology of Down syndrome
- Author(s)
- Antonarakis, SE; Lyle, R; Chrast, R; Scott, HS;
- Details
- Publication Year 2001-10,Volume 36,Issue #2-3,Page 265-274
- Journal Title
- BRAIN RESEARCH REVIEWS
- Publication Type
- Journal Article
- Abstract
- Trisomy 21, which causes Down syndrome, is the model human disorder due to the presence of a supernumerary chromosome. The completion of the sequence of chromosome 21 and the development of appropriate animal models now provide the molecular infrastructure and the reagents to elucidate the molecular mechanisms of the different phenotypes of Down syndrome. The study of the overexpression of single genes, and the dysregulation of global gene expression will enhance the understanding of the pathogenesis of the cognitive impairment of this syndrome. (C) 2001 Elsevier Science B.V. All rights reserved.
- Publisher
- ELSEVIER SCIENCE BV
- Keywords
- TRISOMY-16 MOUSE MODEL; TRANSGENIC MICE; ANIMAL-MODEL; TS65DN MICE; MEIOTIC RECOMBINATION; ABNORMALITIES; HUMAN-CHROMOSOME-21; OVEREXPRESSION; HIPPOCAMPUS; MINIBRAIN
- Publisher's Version
- https://doi.org/10.1016/S0165-0173(01)00103-5
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2001-10-01 12:00:00