The neuropathology of the trisomy 16 mouse.
The purpose of this review is to describe the neuropathology of mouse trisomy 16 and to compare that pathology with the pathologic features observed in individuals with Down syndrome (DS) trisomy 21 (Ts21). Additionally, we will compare the neuroanatomic, neurochemical, and neurophysiologic abnormalities observed in both DS and in mouse trisomy 16 (Ts16). We discuss strategies that have been used to circumvent the failure of trisomy 16 mice to survive into the postnatal period: the creation of chimeras, the use of transplantation of fetal trisomic nervous tissue into normal hosts, and the generation of mice with partial Ts16. We compare the results with those observed in DS and in fetal mouse Ts16. Like individuals with DS, mice with trisomy 16 have triplication of a constellation of genes that have remained together in the same order for roughly 80 million years. As more of these genes have been identified and localized to specific regions of human chromosome 21 and mouse chromosome 16, efforts have been made to create transgenic mice that carry single of these genes in excess. In this review, we also discuss the comparative pathology observed in these transgenic mice.
Lacey-Casem
M L
ML
Division of Biomedical Sciences, University of California, Riverside 92521-0121.
Oster-Granite
M L
ML
D000818:Animals; D001921:Brain / Q000473:pathology*; D002678:Chimera; D004314:Down Syndrome / Q000235:genetics / Q000473:pathology; D006801:Humans; D051379:Mice / Q000235:genetics*; D008822:Mice, Transgenic; D010641:Phenotype; D014314:Trisomy