Skip to main content
Log in

Trisomy 21 and maternal age of menopause: does reproductive age rather than chronological age influence risk of nondisjunction?

  • Short Communication
  • Published:
Human Genetics Aims and scope Submit manuscript

Abstract

The biological basis underlying the increased risk of nondisjunction in offspring of women of advanced maternal age is not understood. We sought to test the hypothesis that maternal reproductive age (distance in time from approaching menopause) rather than chronological age is pivotal in the etiology of nondisjunction. Our results found no difference in age of menopause between women ≥30 years old at delivery of a child with trisomy 21 (i.e., age-related nondisjunction) compared to controls. Among women <30 years of age at delivery of a child with trisomy 21, none underwent premature menopause. Therefore, our findings fail to support the theory that reproductive age plays a major role in the etiology of nondisjunction.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

References

  • Brook JD, Gosden RG, Chandley AC (1984) Maternal aging and aneuploid embryos: evidence from the mouse that biological and not chronological age is the important influence. Hum Genet 66:41–45

    Google Scholar 

  • MacMahon B, Worcester J (1966) Age at menopause, United States 1960–1962. (Vital and health statistics, series 11: Data from the National Health Survey, no 19) (DHEW publication no HSM 66–1000) National Center for Health Statistics, Washington, DC

    Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Rights and permissions

Reprints and permissions

About this article

Cite this article

Phillips, O.P., Cromwell, S., Rivas, M. et al. Trisomy 21 and maternal age of menopause: does reproductive age rather than chronological age influence risk of nondisjunction?. Hum Genet 95, 117–118 (1995). https://doi.org/10.1007/BF00225089

Download citation

  • Received:

  • Revised:

  • Issue Date:

  • DOI: https://doi.org/10.1007/BF00225089

Keywords

Navigation