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Prediction of preeclampsia before 11th week of gestation: a secondary analysis of the ASPIRIN trial
(Elsevier BV, 2025)
Capdeville, Gabriela
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Godinez-Medina, Andrea
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Copado-Mendoza, Diana Y.
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Acevedo-Gallegos, Sandra
;
Rodriguez-Bosch, Mario R.
Background: Early screening for preeclampsia is crucial for preventing adverse maternal and fetal events. Current first-trimester algorithms for predicting preeclampsia are designed to evaluate individual risk between 11.0 and 13.6 weeks of gestation based on various maternal characteristics while integrating biophysical and biochemical features. However, there is limited information regarding risk assessment during earlier stages of pregnancy (i.e., <11.0 weeks gestation). Objective: To develop a prediction model for preeclampsia/eclampsia before 11.0 weeks of gestation as a proof-of-concept in a secondary analysis of the ASPIRIN trial. Study design: This study is a secondary analysis of the ASPIRIN trial, a multinational, randomized, double-blind, placebo-controlled trial. The ASPIRIN trial database, obtained from NICHD DASH, included 11,976 nulliparous pregnant women aged 18–40 with gestational ages of 6.0–13.6 weeks at randomization. Participants were assigned to receive either aspirin (81 mg/day) or placebo until 36.0 weeks or delivery. This secondary analysis included pregnancies delivered at ≥20.0 weeks, excluding those in the aspirin group or with gestational ages ≥11.0 weeks at enrollment. The composite outcome was preeclampsia/eclampsia, as reported in the ASPIRIN trial. Predictor variables available in the dataset included maternal age, education (4 levels), body mass index (BMI kg/m2), gravidity, baseline hemoglobin, baseline systolic blood pressure, and baseline diastolic blood pressure. Logistic regression, with logarithmic transformation for continuous variables, was used to develop the model. The area under the ROC curve with a 95% confidence interval (CI) estimated via bootstrap resampling (1,000 iterations) and the P-value of the Hosmer-Lemeshow statistical test are reported as discrimination and calibration measures. This study used the entire available sample using a complete case approach. Results: A total of 3421 participants met the inclusion criteria, with a cumulative incidence of preeclampsia/eclampsia of 2.9% (99/3,421). Maternal age (21.96 ± 4.13 vs 20.86 ± 3.21, P<.001) and BMI (22.49 ± 4.77 vs 20.79 ± 3.55, P<.001) were significantly higher in the preeclampsia/eclampsia group. Gravidity was lower (P=.023), and hemoglobin levels were slightly elevated (11.88 ± 1.52 g/dL vs 11.50 ± 1.61 g/dL, P=.019) in the preeclampsia/eclampsia group. Educational level (P=.070), systolic blood pressure (P=.720), and diastolic blood pressure (P=.390) showed no significant differences between groups. The logistic regression model yielded an AUC of 0.69 (95% CI 0.63–0.74), and the Hosmer-Lemeshow test P-value was 0.094, indicating acceptable discrimination and calibration. Conclusions: This proof-of-concept logistic regression model using first-trimester maternal characteristics demonstrated acceptable predictive performance for preeclampsia/eclampsia before 11.0 weeks of gestation. During this critical period, several interventions could be proposed to reduce preeclampsia risk, including medication adjustments, lifestyle changes, and appropriate referral if needed. Further studies are required to validate these findings and assess their clinical utility in different settings. © The authors © Elsevier.
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Pathological Nuclear Hallmarks in Dentate Granule Cells of Alzheimer’s Patients: A Biphasic Regulation of Neurogenesis
(2022)
Gil, Laura
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Chi-Ahumada, Erika
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Niño, Sandra A.
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Capdeville, Gabriela
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Méndez-Torres, Areli M.
The dentate gyrus (DG) of the human hippocampus is a complex and dynamic structure harboring mature and immature granular neurons in diverse proliferative states. While most mammals show persistent neurogenesis through adulthood, human neurogenesis is still under debate. We found nuclear alterations in granular cells in autopsied human brains, detected by immunohistochemistry. These alterations differ from those reported in pyramidal neurons of the hippocampal circuit. Aging and early AD chromatin were clearly differentiated by the increased epigenetic markers H3K9me3 (heterochromatin suppressive mark) and H3K4me3 (transcriptional euchromatin mark). At early AD stages, lamin B2 was redistributed to the nucleoplasm, indicating cell-cycle reactivation, probably induced by hippocampal nuclear pathology. At intermediate and late AD stages, higher lamin B2 immunopositivity in the perinucleus suggests fewer immature neurons, less neurogenesis, and fewer adaptation resources to environmental factors. In addition, senile samples showed increased nuclear Tau interacting with aged chromatin, likely favoring DNA repair and maintaining genomic stability. However, at late AD stages, the progressive disappearance of phosphorylated Tau forms in the nucleus, increased chromatin disorganization, and increased nuclear autophagy support a model of biphasic neurogenesis in AD. Therefore, designing therapies to alleviate the neuronal nuclear pathology might be the only pathway to a true rejuvenation of brain circuits.
Scopus© Citations 6 10 2
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Aging and Alzheimer’s disease connection: Nuclear Tau and lamin A
(2021)
Gil, Laura
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Niño, Sandra A.
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Capdeville, Gabriela
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Jiménez-Capdeville, María E.
Age-related pathologies like Alzheimer`s disease (AD) imply cellular responses directed towards repairing DNA damage. Postmitotic neurons show progressive accumulation of oxidized DNA during decades of brain aging, which is especially remarkable in AD brains. The characteristic cytoskeletal pathology of AD neurons is brought about by the progressive changes that neurons undergo throughout aging, and their irreversible nuclear transformation initiates the disease. This review focusses on critical molecular events leading to the loss of plasticity that underlies cognitive deficits in AD. During healthy neuronal aging, nuclear Tau participates in the regulation of the structure and function of the chromatin. The aberrant cell cycle reentry initiated for DNA repair triggers a cascade of events leading to the dysfunctional AD neuron, whereby Tau protein exits the nucleus leading to chromatin disorganization. Lamin A, which is not typically expressed in neurons, appears at the transformation from senile to AD neurons and contributes to halting the consequences of cell cycle reentry and nuclear Tau exit, allowing the survival of the neuron. Nevertheless, this irreversible nuclear transformation alters the nucleic acid and protein synthesis machinery as well as the nuclear lamina and cytoskeleton structures, leading to neurofibrillary tangles formation and final neurodegeneration.
Scopus© Citations 18 30 1

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