Down syndrome, caused by the triplication of human chromosome 21, is the most frequent genetic cause of mental retardation. Mice with a segmental trisomy for mouse chromosome 16, which is orthologous to human chromosome 21, exhibit abnormalities similar to those in individuals with Down syndrome and therefore offer the opportunity for a genotype-phenotype correlation. In the current review, I present several mouse lines with trisomic regions of various lengths and discuss their usefulness for elucidating the mechanisms underlying Down syndrome-associated developmental cognitive disabilities. In addition, our recent comprehensive study attempting to identify molecules with disturbed expression in the brain of a mouse model of Down syndrome in order to develop a pharmacologic therapy for Down syndrome is described.
CITATION STYLE
Ishihara, K. (2017). Comprehensive analyses of molecules with altered expression in the brain of a mouse model of down syndrome for identification of pharmacotherapeutic targets. Yakugaku Zasshi. Pharmaceutical Society of Japan. https://doi.org/10.1248/yakushi.16-00236-3
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