European journal of obstetrics, gynecology, and reproductive biology · 2026
Developmental kinetics distinguish meiotic from mitotic chromosomal defects: Day-5 blastocyst achievement as age-independent predictor of euploid embryo yield.
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Hung Mai Vuong, Hai Ha Pham Thi, Han Hoan Nguyen Khac, Luan Nguyen Thanh
Аннотация
BACKGROUND: While maternal age is established as a dominant reproductive risk factor, the mechanistic distinction between age-dependent meiotic errors and age-independent mitotic errors remains uncharacterized. These divergent pathways have profound implications for patient counseling and treatment stratification but are rarely differentiated clinically.
OBJECTIVES: To establish distinct etiological pathways underlying chromosomal abnormalities by quantifying the differential age-sensitivity of whole-chromosome aneuploidies (meiotic origin) versus mosaic abnormalities (mitotic origin), determining whether developmental timing serves as an age-independent biomarker of genomic competence, and enabling practitioners to provide pathway-specific counseling and treatment recommendations.
SEARCH STRATEGY: PubMed, Embase, and ClinicalTrials.gov were searched for relevant studies.
SELECTION CRITERIA: Retrospective cohort of 490 IVF patients (2,472 embryos) stratified by maternal age (≤35, 35-40, ≥40 years) with complete extended culture and next-generation sequencing (NGS)-based preimplantation genetic testing for aneuploidy.
DATA COLLECTION AND ANALYSIS: Age-stratified analysis of developmental kinetics and comprehensive chromosomal classification. Multivariate logistic regression identified independent predictors of aneuploidy, adjusting for maternal age and day-5 blastocyst count.
MAIN RESULTS: Whole-chromosome aneuploidies demonstrated striking age-sensitivity (14.0 % to 36.5 %, 2.6-fold increase, p < 0.001), reflecting progressive cohesin complex degradation, spindle checkpoint decline, and mitochondrial bioenergetic insufficiency. Mosaicism remained age-independent (∼41 %, p = 0.383), arising from post-meiotic mitotic errors. Day-5 blastocyst formation declined 30 % with age (p = 0.0154), yet day-6 formation remained age-independent (p = 0.106), indicating developmental delay rather than failure. Day-5 blastocyst count independently protected against aneuploidy (OR 0.965, 95 % CI: 0.944-0.987, p = 0.002), persisting after multivariate adjustment.
CONCLUSIONS: Mechanistic differentiation between age-dependent meiotic and age-independent mitotic chromosomal abnormalities reveals fundamentally distinct etiological pathways with profound implications for clinical decision-making. In particular, day-5 blastocyst achievement emerges as an independent biomarker of oocyte quality, enabling precise within-age-group risk stratification regardless of chronological age. These findings translate developmental kinetics into quantitative clinical algorithms that substantially improve reproductive counseling accuracy and patient-specific prognostication beyond traditional age-based approaches.
OBJECTIVES: To establish distinct etiological pathways underlying chromosomal abnormalities by quantifying the differential age-sensitivity of whole-chromosome aneuploidies (meiotic origin) versus mosaic abnormalities (mitotic origin), determining whether developmental timing serves as an age-independent biomarker of genomic competence, and enabling practitioners to provide pathway-specific counseling and treatment recommendations.
SEARCH STRATEGY: PubMed, Embase, and ClinicalTrials.gov were searched for relevant studies.
SELECTION CRITERIA: Retrospective cohort of 490 IVF patients (2,472 embryos) stratified by maternal age (≤35, 35-40, ≥40 years) with complete extended culture and next-generation sequencing (NGS)-based preimplantation genetic testing for aneuploidy.
DATA COLLECTION AND ANALYSIS: Age-stratified analysis of developmental kinetics and comprehensive chromosomal classification. Multivariate logistic regression identified independent predictors of aneuploidy, adjusting for maternal age and day-5 blastocyst count.
MAIN RESULTS: Whole-chromosome aneuploidies demonstrated striking age-sensitivity (14.0 % to 36.5 %, 2.6-fold increase, p < 0.001), reflecting progressive cohesin complex degradation, spindle checkpoint decline, and mitochondrial bioenergetic insufficiency. Mosaicism remained age-independent (∼41 %, p = 0.383), arising from post-meiotic mitotic errors. Day-5 blastocyst formation declined 30 % with age (p = 0.0154), yet day-6 formation remained age-independent (p = 0.106), indicating developmental delay rather than failure. Day-5 blastocyst count independently protected against aneuploidy (OR 0.965, 95 % CI: 0.944-0.987, p = 0.002), persisting after multivariate adjustment.
CONCLUSIONS: Mechanistic differentiation between age-dependent meiotic and age-independent mitotic chromosomal abnormalities reveals fundamentally distinct etiological pathways with profound implications for clinical decision-making. In particular, day-5 blastocyst achievement emerges as an independent biomarker of oocyte quality, enabling precise within-age-group risk stratification regardless of chronological age. These findings translate developmental kinetics into quantitative clinical algorithms that substantially improve reproductive counseling accuracy and patient-specific prognostication beyond traditional age-based approaches.