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Maternal age in trisomy.

N E Morton1, P A Jacobs, T Hassold

  • 1Department of Community Medicine, University of Southampton, Southampton General Hospital, England.

Annals of Human Genetics
|July 1, 1988
PubMed
Summary
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Maternal age influences trisomy risk, with most trisomies independent of age. However, some trisomies, like Trisomy 16, are strongly age-dependent, suggesting complex origins for chromosomal abnormalities.

Area of Science:

  • Genetics
  • Reproductive Biology
  • Biostatistics

Background:

  • Trisomy, a condition of having an extra chromosome, is a significant factor in live births, spontaneous abortions, and during prenatal diagnosis via amniocentesis.
  • Maternal age is a known risk factor for certain trisomies, but the precise relationship and underlying mechanisms are complex and not fully elucidated.

Purpose of the Study:

  • To analyze the relationship between maternal age and the frequency of trisomy across different reproductive outcomes.
  • To differentiate between age-dependent and age-independent pathways contributing to trisomy formation.
  • To investigate exceptional cases, such as Trisomy 16, to understand unique etiological factors.

Main Methods:

  • Statistical modeling, specifically fitting a logistic model augmented by an age-independent proportion, to trisomy data stratified by maternal age.

Related Experiment Videos

  • Analysis of data from live births, amniocenteses, and spontaneous abortions.
  • Comparison of trisomy frequencies across different chromosome groups and specific trisomies (e.g., Trisomy 16, 22).

    • Main Results:

    • Trisomy frequency generally increases monotonically with maternal age, without significant deviations at very young or very old maternal ages.
    • A substantial proportion of trisomies, particularly for groups A, B, and C chromosomes, arise from processes independent of maternal age.
    • Trisomy 16 was found to be exceptional, with all cases appearing to be age-dependent.
    • A smaller fraction of trisomies, including about half of those for smaller chromosomes (excluding 16 and possibly 22), are dependent on maternal age, suggesting a process independent of paternal age and crossing-over.

    Conclusions:

    • The data support a model where trisomy arises from both age-dependent and age-independent mechanisms.
    • The distinct pattern of Trisomy 16 highlights specific etiological pathways for certain chromosomal abnormalities.
    • Understanding these distinct pathways is crucial for accurate risk assessment and potential interventions in reproductive genetics.