| First Author | Leffler A | Year | 1999 |
| Journal | Ann Anat | Volume | 181 |
| Issue | 3 | Pages | 247-52 |
| PubMed ID | 10363106 | Mgi Jnum | J:102797 |
| Mgi Id | MGI:3608080 | Doi | 10.1016/S0940-9602(99)80039-9 |
| Citation | Leffler A, et al. (1999) Germ cell migration and early development of the gonads in the trisomy 16 mouse--an animal model for Down's syndrome. Ann Anat 181(3):247-52 |
| abstractText | The aneuploid condition of patients with Down's syndrome (trisomy 21) frequently leads to a sub- or infertility of these individuals. Gonads from adults and fetuses with trisomy 21 demonstrated histologically a remarkable reduction in germ cells. Disorders in the germ cell migration, the early development of the gonads as well as meiotic defects are thought to contribute to this pathomorphology. To gain information about premeiotic defects, investigations on the trisomy 16 mouse, an animal model for Down's syndrome, were carried out. By means of morphometric studies a delay in migration and a reduction in primordial germ cells was evaluated in trisomic mice of embryonic day 11 (E11). At day E13 a generalized growth retardation of the developing gonads was obvious in trisomic animals. Additionally performed electron microscopic examinations revealed signs of germ cell demise in trisomy 16 mice. Thus, the mechanisms of a diminished proliferation capacity, impaired migration and premature death of germ cells represent premeiotic disorders that presumably contribute to the pathomorphology observed in the gonads of individuals with Down's syndrome. |
