Down’s syndrome (DS), caused by trisomy 21, is the most commonly identified form mental retardation with a frequency of up to 1 in 600-800 births [1]. It has been estimated that the largest part of trisomy 21 fetuses are aborted during the first trimester of pregnancy (1 in 150 of all pregnancy losses) [2]. Therefore, this chromosome abnormality is considered as one of the most important genetic anomalies in humans. The results of several studies have shown that the majority of anomalies leading to tri­somy 21 being due to errors in the egg, as 90% of the additional chromosome 21 is of maternal origin. About 10% are of paternal origin, and a much lower percentage of trisomy 21 is attributed to post-zygotic mitotic non-disjunction [3]. Petersen and Mikkelsen [4] report that the contribution of paternal meiotic errors leading to trisomy 21 is estimated as 5.5%, and post-zygotic mitotic non-disjunction as 3.8%. Thus, this point still remains unclear. Whereas altered recombination is accepted as an observa­tion in non-disjunction of chromosome 21, the underlying causes and mechanisms of this phenomenon are unknown. There is a suggestion that several errors (abnormal spindle formation, premature release of sister chromatid adhesion), each having a small effect on the processes of meiosis, lead to non-disjunction, and that different processes are responsible for various non-disjunction subtypes.