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Amplified developmental instability in Down's syndrome.

B L Shapiro

    Annals of Human Genetics
    |May 1, 1975
    PubMed
    Summary
    This summary is machine-generated.

    The extra chromosome in Down syndrome (DS) amplifies developmental instability. Palatal dimensions and atd angle show greater abnormality in DS, indicating widespread developmental deviations.

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    Area of Science:

    • Genetics
    • Developmental Biology
    • Human Anatomy

    Background:

    • Down syndrome (DS) is associated with an extra chromosome 21.
    • Developmental canalization, the buffering of development against genetic and environmental perturbations, may be impaired in DS.
    • Understanding developmental instability in DS is crucial for identifying specific affected systems.

    Purpose of the Study:

    • To investigate the hypothesis that DS leads to a generalized decrease in developmental canalization.
    • To compare palatal dimensions and atd angle variability in DS subjects and controls.
    • To determine if traits with higher environmental sensitivity in the general population are disproportionately affected in DS.

    Main Methods:

    • Measurement of three palatal dimensions (height, width, anteroposterior length) in DS subjects and controls.

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  • Twin analyses to assess the contribution of environmental factors to palatal dimension variability.
  • Comparison of the maximum atd angle in DS subjects and controls.

    • Main Results:

    • Palatal length exhibited the greatest environmental contribution to variability in twin analyses.
    • Palatal length was the most abnormal dimension among the three measured in DS subjects.
    • The maximum atd angle was significantly more deviant from normal in DS subjects compared to controls.

    Conclusions:

    • The findings support the hypothesis of generalized amplified developmental instability in Down syndrome.
    • Traits with higher environmental sensitivity appear to be disproportionately affected in DS.
    • These results suggest a widespread disruption of developmental buffering mechanisms in DS.