Effects of maternal ageing on developmental defects in mice.

Greenwood et al.1) used the expression, "experimental epidemiology" for the laboratory study on animal diseases analogous to human complaints. A controlled experiment in which one variable is manipulated is essential in order to test a hypothesis of disease etiology. An animal model of human diseases has been used extensively in order to discover the mechanism that spreads infectious diseases. In more recent times a major problem of experimental epidemiology is not only in infectious diseases, but also in non-infectious chronic ones, even including developmental defects.2) The risk of occurrence of chromosome anomalies, particularly those in Down syndrome, increases as a woman reaches the later years of reproductive life. This is interpreted as due to increased chromosomal non-disjunction in aged oocytes.3) It is therefore of interest to examine the frequency of chromosome anomalies in embryos of aged animals. If such a maternal dependence could be established in experimental animals, it may be possible to distinguish extrinsic effects on chromosomal non-disjunction from intrinsic factors of ageing in order to investigate the etiology of Down syndrome more closely. Several attempts have been made to learn whether there is a correlation between incidence of chromosome anomalies and maternal aging in animals. Goodlin4) reported no increased aneuploidy in newborns of aged mice. Recently Yamamoto et al.5) reported a high incidence of chromosome anomalies in embryos of aged mice by employing an improved method for cytogenetic analysis during midgestation. This paper deals with consecutive chromosome analyses of embryos of female mice 2-16 months old.